الفهرس 
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Abstract
In conclusion, this study suggests that in CHC patients infected with HCV genotype 4, a direct effect of the virus may result in decreased adiponectin levels. The latter is further supported by the significant increase in adiponectin levels in HCV genotype 3-infected patients at the end of treatment compared with their pretreatment levels. Serum adiponectin and TNF-α at baseline seem to be independent predictors of liver steatosis irrespective of HCV genotype, while adiponectin is also an independent predictor of the achievement of end-of-treatment virological response. Further multicenter studies are needed, however, including a larger number of CHC patients, in order to confirm our results and to address whether our findings have any pathophysiological significance in the HCV disease course. In addition, we believe that further efforts should be made in an attempt to corroborate our findings regarding SVR, and to evaluate the possible usefulness of a potential increase in serum adiponectin using novel molecules (e.g., recombinant forms of adiponectin) or using treatments leading to an increase in adiponectin (e.g., thiazolidinediones) before the initiation of antiviral treatment in CHC patients, though a very recent report showed that significant changes in adipocytokines during treatment of HCV patients were unrelated to virological outcome.