The thesis based on a comprehensive histopathological, histochemical, immunohistochemical and morphometric study of trephine biopsy of the liver of patients and analysis of their laboratory and biochemical evidence-based definition of the basic concept of pathological modalities progression of chronic viral hepatitis B, C and B + C with the virus caused destruction of hepatocytes, expression of immune cellular destruction and the degree and type of liver fibrosis. Is proved the necessity of an individual approach to the postmortern examination of the liver aimed at determining the variability of course of CVH and its progression, depending on the genotype of the pathogen, the state of reactivity of the microorganism and the patient's response to antiviral therapy. On the basis of pathologic analysis of biopsies and laboratory biochemical parameters revealed that the most unfavorable course of CVH C observed in patients with genotype 1b hepatitis C virus. Convincingly shown that in the progression of chronic viral hepatitis dominant importance has immunocytic killing of hepatocytes and immune cellular liver destruction in the areas of "step and bridging necrosis" by aggressive specialized immune cells (CD8+ T cells, CD68+ macrophages, Kupffer cells, pit-cells) with the participation of CD5+ lymphocytes, CD20+ B-lymphocytes and CD45R0+ T-lymphocytes. Immunohistochemical methods demonstrated that in the progression of chronic viral hepatitis B, C and B + C negative role played not only by portal-septal, but perisinusoidal-centrolobular and mixed liver fibrosis, predictive of which is increase of perisinusoidal ?-SMA+ cells and ?-SMA+ fibroblasts in the portal tracts and periportal zones followed excessive collagen synthesis by these cells collagen I, III and type IV, as well as a high level in blood serum TGF-?1 and hyaluronic acid. Determined that progression of fibrosis of the liver from mild F1 to severe F3 extent in patients who have not responded to the AVT, compared with virological responders, registered 6.6 times more often in chronic viral hepatitis C and 2 times more often in chronic viral hepatitis B, so after 5 years AVT after progression of liver fibrosis is found in 41.7% of patients with chronic viral hepatitis C and in 33.3% of patients with chronic viral hepatitis B. Morphometrical and immunohistochemical methods revealed that the progression of fibrosis of the liver moderate F2 to severe F3 when raising portal-septal fibrosis in liver was significantly increased in half accumulation of collagen type I and twice - collagen type III, when a mixed - portal-perisinusoidal-centrolobular fibrosis in the liver was significantly increased in 2.5 times accumulation of collagen type I and half - type III collagen. Thus, we confirm that the current stage of chronic viral hepatitis B, C and B+C most reliably reflects a certain degree of fibrosis in liver biopsies. On the basis of 10 years of clinical and pathologic monitoring of liver biopsies in patients with chronic viral hepatitis, morphological studies of repeated biopsies of the liver, analysis of hepatotropic viral genotype and comparative analysis of laboratory biochemical parameters in patients with an interval of 5 years proven that most often the result of chronic viral hepatitis is the development of liver cirrhosis in 25,67% patients and less - the development of liver cancer in 12,28% patients and long-term remission of chronic viral hepatitis in 0,67% patients. First established that progression of cirrhosis leads to syndrome of severe portal hypertension happens in patients with chronic viral hepatitis who had not received antiviral therapy, primarily caused by the subsequent immune cellular destruction of liver pseudolobules and increased fibrosis less - to necrosis of pseudolobules due to intrahepatic shunting of blood. In patients with chronic viral hepatitis describes the main histological types of hepatocellular carcinoma of the liver, which is determined by immunohistochemical expression of hepatocyte marker Hepatocyte. It is proved that the expression of cancer cells HBcAg and HBsAg the most convincing evidence the relationship of liver cancer and chronic viral hepatitis B. Found that the pathologic features of remission of chronic viral hepatitis is the lack immunocytic "step and bridging necrosis" and a significant amount of ?-SMA+ cells in the perisinusoidal spaces and in the portal tracts of the liver, as well as the degree of stabilization of liver fibrosis.
