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Abstract
Chronic infection with the hepatitis C virus (HCV) is a major cause of progressive liver damage, whose long-term sequellae include cirrhosis and hepatocellular carcinoma (Niederau et al.,1998).
The rate of histological and clinical progression of chronic hepatitis C is variable, depending on the presence of several cofactors including age at infection, gender, prolonged alcohol abuse and co-infections with the hepatitis B virus or the human immunodeficiency virus (Kenny-Walsh,1999).
Liver steatosis is a frequent finding in chronic hepatitis C. An association has been suggested between steatosis and fibrosis progression rate, but the pathogenetic mechanisms linking fatty infiltration and collagen deposition are unknown (Adinolfi et al.,2001).
Current data suggest that there are at least two types of steatosis in HCV patients:
(1) Virally-related steatosis, which correlates with HCV replication level, is often associated with genotype 3, and disappears upon successful antiviral therapy (Rubbia-Brandt et al.,2000)
(2) Metabolic steatosis, whose presence and severity correlate with body mass index (BMI), and that does not respond to antiviral treatment, even in virological responders (Patton et al.,2004).
Among patients infected with hepatitis C virus (HCV), 13-33% develop type 2 diabetes mellitus whether this reflects an HCV-mediated effect remains to be established (Knobler et al.,2003).
(Konrad et al.,2000) and( Maeno et al.,2003) reported that HCV-infected patients with normal glucose tolerance are insulin resistant and this insulin resistance appears to be closely related with the severity of HCV-induced liver damage.
(Hui et al.,2003);( Hickman et al.,2003) and (Ratziu et al.,2003) research results have linked for the first time insulin resistance—but not steatosis—to fibrosis in patients with chronic hepatitis C and that insulin resistance syndrome capable of influencing the degree of both steatosis and fibrosis in chronic hepatitis C .These observations are important in view of the debated role of HCV infection in the establishment of an insulin resistant state.The above mentioned studies also suggest the presence of a factor (?HCV) other than overweight and/or obesity involved in the pathogenesis of insulin resistance.
According to (Alba et al.,2005) ; steatosis and insulin resistance may be fibrogenic independently of each other. This is also compatible with recent experimental data, showing that the expression of the HCV core protein in mice is directly responsible of insulin resistance and that this event precedes the appearance of steatosis in the liver (Shintani et al.,2004).