The process of liver fibrosis in chronic hepatitis C - histological and immunohistochemical study.

Liver fibrosis is one of the most serious histopathological (HP) lesions that, together with the inflammatory process and the hepatocyte lesions, determine the change of the liver architecture, having as a clinical result the onset of liver failure phenomena. Hepatitis C virus represents one of the most frequent conditions leading to the onset of liver fibrosis and favors the progression of the disease towards hepatocellular carcinoma. We evaluated the HP and immunohistochemical (IHC) aspects on fragments of liver biopsies taken from 104 patients diagnosed with chronic hepatitis C and altered capacity of work. In our study, we observed a growth of the portal (Kiernan) spaces by the presence of a chronic inflammatory infiltrate, the presence of collagen fibers and conjunctive matrix. The density and dimensions of collagen fibers were correlated with the severity of the liver disease, in the severe forms being highlighted porto-portal and porto-central fibrous bridges. The IHC examinations highlighted the change of the phenotype of perisinusoidal dendritic cells, the growth of the myofibroblast cells in the portal spaces, the growth of the macrophage number in the inflammatory infiltrate and of the Kupffer cells in the liver parenchyma.

Anatomo-clinical correlations in hepatic steatosis in patients with C chronic hepatitis.

Hepatic steatosis is a progressive liver disease, frequently met in chronic virus C hepatitis, playing an important role in its evolution towards fibrosis, necroinflammation and the final stage the hepatocellular carcinoma. The present paper studies the correlation between clinico-epidemiological parameters and the pathology test outcome in patients with hepatic biopsies carried out before they began the antiviral treatment. We used the classical histological staining and the immunolabeling. The presence of steatosis is not directly associated with clinico-epidemiological parameters and with the degree of fibrosis and inflammation.

Antifibrotic action of telmisartan in experimental carbon tetrachloride-induced liver fibrosis in Wistar rats.

BACKGROUND AND AIMS: Liver fibrosis is the increasingly accumulation of extracellular matrix (ECM), caused by chronic liver injuries, and represents a difficult clinical challenge in the entire world. Currently, the advanced knowledge of the cellular and molecular mechanisms of liver fibrosis showed that collagen-producing cells, like activated hepatic stellate cells (HSCs), portal fibroblasts and myofibroblasts are activated by fibrogenic cytokines, such as angiotensin II, transforming growth factor-beta 1 (TGF-ß1), and leptin. Because of these, we tested telmisartan, an angiotensin II (AT1) receptor blocker and a peroxisome proliferator-activated receptor-γ (PPARγ) partial agonist, for investigate its antifibrotic action, on experimental model of carbon tetrachloride-induced liver fibrosis. MATERIALS AND METHODS: In this research, we used two groups of Wistar rats, which received intraperitoneal (i.p.) injection of carbon tetrachloride (CCl4) 40% dissolved in olive oil, twice weekly for four consecutive weeks (initial dose of 5 mL÷kg, and other doses 3 mL÷kg). After one week, one group was received by gavage telmisartan (TS) dissolved in saline 0.9%, daily in dose of 8 mg÷kg, for 28 days. One group of Wistar rats was used for control. The antifibrotic action of telmisartan was investigated on the pathological changes of the liver and immunohistochemical analysis for hepatic stellate (Ito) cells (HSCs) reaction using anti-alpha-smooth muscle actin (anti α-SMA) antibody and macrophages cells (Kupffer cells) reaction using anti-CD68 antibody. RESULTS AND CONCLUSIONS: In group treated with telmisartan, hepatic fibrogenesis process was significantly reduced, in comparison with CCl4 group.