الفهرس 
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Abstract
Hepatitis C virus (HCV) is a small, single-stranded, positive-sense, RNA virus that belongs to the Hepacivirus genus of the Flaviviridae family. Six major genotypes and about 30 subtypes have been identified; Genotype 4 is found primarily in the Middle East and sub-Saharan Africa (Antonelli et al., 2009).The WHO has declared hepatitis C global health problem with approximately 3 % of world population (roughly 170-200 million people) infected with HCV (Miller et al., 2010). In Egypt the situation is quite worse as it has the highest prevalence of HCV in the world. The released Egyptian Demographic Health Survey [EDHS]* tested a representative sample of the entire country for HCV antibody. The overall prevalence (percentage of people) positive for antibody to HCV was 14.7% (El-Zanaty et al., 2009 The current treatment for patients with chronic hepatitis C (CHC) is Interferon-based therapy in combination with Ribavirin for 24 to 48 weeks (Manns et al., 2006). Rapid virologic response (RVR), defined as an undetectable serum hepatitis C virus (HCV) RNA level at week 4 of treatment, is emerging as an important milestone in the treatment of patients who have chronic hepatitis C by use of pegylated interferon alfa and ribavirin—the current standard of care (Poordad et al., 2008 The mechanisms underlying the failure of interferon therapy are not well understood, but evidence indicates that in addition to viral factors, several host factors are also involved (Gao et al., 2004 Insulin resistance is defined as a condition in which higher than normal insulin concentrations are needed to achieve normal metabolic responses or alternatively, normal insulin concentrations are unable to achieve normal metabolic responses (Bugianesi et al., 2005 Insulin resistance emerges as a very important host factor in patients with chronic hepatitis C, mainly because it has been related to steatosis development, fibrosis progression and non response to peginterferon plus ribavirin. Insulin resistance appears as a consequence of the inability of insulin to induce the effect on glucose metabolism and an abnormally large amount of insulin is secreted to achieve a biological response. The hyperinsulinemic state induces several abnormalities in the liver, endothelium, and kidneys, and is the main feature in the metabolic syndrome (Romero-Gómez, 2006 Insulin resistance is one of the pathogenic factors in the development of steatosis in chronic hepatitis C, both viral induced insulin resistance and metabolic induced insulin resistance could be implied in the development of steatosis. The main deleterious effect of insulin resistance in chronic hepatitis C is the ability to promote fibrosis progression (Ratziu et al., 2003).Mean homeostasis model assessment index increases with the stage of fibrosis and could help to differentiate stages of fibrosis (Fartoux et al., 2005). Insulin resistance, calculated by the homeostasis model assessment (HOMA), has been found to impair virological response to combined therapy in chronic hepatitis-C patients (Romero-Gomez et al., 2005).