Immunohistochemical characteristics of collagen I, III, IV type deposition in the dynamics of progressing of the basic types of liver fibrosis in patients with non-alcohol steatohepatitis.

Abstract

Background. The study of patterns of collagen deposition of various types in the dynamics of hepatic fibrosis progression is essential to the development of targeted therapy for liver fibrosis in patients with nonalcoholic and alcoholic steatohepatitis. Objective. The aim is to study the area of deposition of collagen I, III and IV type in the dynamics of the progression of F 1 - F 3 perisinusoidal-pericellular and portal-perisinusoidal fibrosis in F 4 liver cirrhosis of micronodular and pericellular type in hepatotrepanobioptates of patients with nonalcoholic steatohepatitis, using the methods of immunohistochemistry. Methods. The immunohistochemical studies are conducted in liver trepanobioptates in 80 patients with perisinusoidal pericellular and portal perisinusoidal fibrosis of varying severity. Results. It is found that the deposition of type I, III and IV collagen increases with the development and progression of fibrosis from F1 – the weak grade, to F2 –the moderate grade and F3 to severe grade of fibrosis in the liver. With the progression of perisinusoidal pericellular and portal perisinusoidal fibrosis, the increase in type III collagen deposition decreases. In F4 liver fibrosis/cirrhosis of the pericellular type, the deposition of type I and IV collagen reaches a maximum, the area of deposition of type I collagen is more than 50% greater than the deposition area of type III collagen. In F4 fibrosis/cirrhosis of the portal perisinusoidal type, the deposition area of type I collagen also reaches a maximum, while the collagen storage area of type III and IV stabilizes at the level of severe F3 of liver fibrosis. Conclusion. In patients with nonalcoholic steatohepatitis, the quantitative ratios of different types of collagen in the zones of perisinusoidal pericellular and portal perisinusoidal fibrosis change dynamically as the hepatofibrosis increase and its transformation into liver cirrhosis.