The natural course of liver fibrosis in non-alcoholic fatty liver disease and after chronic hepatitis C cure in patients with normal body weight and obesity
Abstract
Liver cirrhosis and fibrosis is an increasing medical problem all over the world. Several decades ago, hepatitis C infection was the main cause of liver cirrhosis and severe liver fibrosis. After the change of antiviral treatment strategy, we have non-alcoholic fatty liver disease as the main origin factor of liver cirrhosis. After effectively eliminating hepatitis C virus, many patients still have residual post-hepatitis fibrosis. In case of accompanying non-alcoholic fatty liver disease, the natural course of liver lesion is the progress of fibrosis. The presented article highlights the main methods of post-hepatitis liver fibrosis diagnostics after curing viral hepatitis type C and in patients with non-alcoholic fatty liver disease affected by overweight and obesity. We have evaluated fibrosis development with serum markers such as FIB-4, FibroTest and transforming growth factor β1 level. Post-hepatitis liver fibrosis status after elimination of viral hepatitis type C should be observed, especially in patients with non-alcoholic fatty liver disease. FIB-4 and FibroTest correlate with each other and with biochemical liver indices and generally depend on overweight and obesity. TGF-β blood level significantly increases in case of fibrosis progression with maximum values in the group of patients with NAFLD and BMI level above 30 kg/m2 (p<0.05). In the case of liver fibrosis progression, the concentration of TGF-β1 in blood increases (r=0.78, p<0.05). It confirms the role of this cytokine in the activation of hepatic stellate cells and stimulation of the synthesis of collagen and other extracellular fibrotic components and can be a marker of NAFLD progression.