الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Background: Liver fibrosis can be considered as a dynamic and highly integrated cellular response to chronic liver injury. At the molecular level, growth factors, cytokines and chemokines, changes in ECM organization and composition as well as reactive molecules originated by oxidative stress have been suggested to play a pathogenetic role. Transforming growth factor- 1 is believed to be a potential molecular link between the inflammatory process and fibrosis. In hepatic fibrogenesis, TGF- 1 is thought to activate lipocytes in the liver, which then produce the extracellular matrix proteins involved in the formation of fibrosis Aim of the work: The present study has aimed to determine the pathogenic and pathognomonic roles of the transforming growth factor as well as oxidative stress in chronic liver disease, also to correlate the changes of these parameters with staging of liver affection. This study evaluate also hepatocyte proliferation using MIB1-Ki67 labeling index in histological examination of different causes of chronic liver disease. Method: This case control study was carried out on cases attending clinics of Tropical Medicine Unit (inpatient and outpatient) Mansoura University Hospital. This study included 80 patients with chronic liver disease, those subjects were randomly selected. In addition to 10 healthy control which matched age and sex with the test group. The studied cases were classified into the following groups: Group 1: Hepatitis C virus (HCV) positive group. Group 2: Hepatitis B virus (HBV) positive group. Group 3: Patients with non-alcoholic steato-hepatitis (NASH). Group 4: Patients with hepato-cellular carcinoma. Group 5: Patients with schistosomal hepatic fibrosis. Group 6: control group. Results: As regard MDA level, there were significant difference in control group versus the studied groups as following: patients of either HCV or HBV related liver diseases (patients with chronic hepatitis C either normal or elevated enzymes, chronic hepatitis B, and patients with post HCV, post HBV decompensated cirrhosis) (P = 0.006, 0.007, 0.025, 0.027, 0.003 respectively), and NASH group and hepatocellular carcinoma group (P = 0.001, 0.008 and 0.002 respectively), while in Schistosomal hepatic fibrosis group there was non significant (P = 0.406 ). As regard serological TGF- level, there were significant difference in control group versus the studied groups as following: patients of either HCV or HBV related liver diseases (patients with chronic hepatitis C either normal or elevated enzymes, chronic hepatitis B, and patients with post HCV, post HBV decompensated cirrhosis) (P = 0.001, 0.000, 0.001, 0.000, 0.002 respectively), and NASH group, hepatocellular carcinoma group and Schistosomal hepatic fibrosis group (P = 0.000, 0.001 and 0.002 respectively). Also, there were significant difference as regard serological TGF- level when comparing Child C versus either Child B (P = 0.012) or Child A (P = 0.045), while there was non significant difference when comparing Child A versus Child B (P = 0.804). Conclusions: Oxidative stress is a feature of different diseases of chronic liver damage suggests a possible role in their pathogenesis. Oxidative stress represents an early event in chronic HCV infection as evidenced by the high level of MDA in all presentations of hepatitis c infection. TGF- was significantly correlated with fibrosis score. This is denoting that TGF- highly involved in the pathogenesis of liver fibrosis. TGF- could be considered as a molecular link between the inflammatory process and progression of fibrosis as it is highly correlated with both fibrosis score and modified histological activity index. Necroinflammatory injury mostly associated with higher proliferative index that reflect increased susceptibility of these patients for progression to dysplastic changes. So, arrangement of the therapy for them should be considered as a ranging for fibrosis stages.