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AIM:To determine whether body weight and/or serumleptin were independent predictors of response toantiviral treatment in patients with chronic hepatitis C.METHODS:A retrospective evaluation was performedin 139 patients with chronic hepatitis C treated withinterferon(IFN)from 1996 to 2000.Sustained responsewas defined as negative by hepatitis C virus(HCV)RNAanalysis using PCR and normal transaminase at 24 wkafter cessation of IFN therapy.Patients who remainedpositive for HCV RNA at the end of IFN treatment weredefined as resistant to IFN therapy.Sex,age,body massindex(BMI)(≥25 vs<25),complication of diabetesmellitus,serum leptin level(≥8.0 μg/L vs<8.0 μg/L),and the stage of liver fibrosis by needle biopsy(F1/F2 vsF3/F4)were examined.RESULTS:Sustained response was achieved in 33patients(23.7%),while others failed to show a responseto IFN therapy.Overall,the factors associated withsustained antiviral effects were HCV-RNA load,HCVgenotype,serum leptin level,and stage of liver fibrosisevaluated by univariate analysis.BMI was not associatedwith any therapeutic effect of IFN.Multivariate analysisindicated that HCV-RNA load was a significant risk factor,but among the patients with low viremia(HCV-RNA<100 MU/L),leptin level was an independent risk factorfor IFN resistance.Namely,a high level of serum leptinattenuated the effect of IFN on both male and femalepatients with low viremia.CONCLUSION:High serum leptin level is a negative predictor of response to antiviral treatment in chronichepatitis C with low viremia.
AIM: To determine whether body weight and / or serum leptin were independent predictors of response to antiviral treatment in patients with chronic hepatitis C. METHODS: A retrospective evaluation performed performed in 139 patients with chronic hepatitis C treated within interferon (IFN) from 1996 to 2000. defined as negative by hepatitis C virus (HCV) RNA analysis using PCR and normal transaminase at 24 wkafter cessation of IFN therapy. Patients who remain positive for HCV RNA at the end of IFN treatment weredefined as resistant to IFN therapy. Ex, age, body mass index BMI) (≥25 vs <25), complication of diabetes mellitus, serum leptin level (≥8.0 μg / L vs <8.0 μg / L), and the stage of liver fibrosis by needle biopsy (F1 / F2 vsF3 / F4) .RESULTS: Sustained response was achieved in 33 patients (23.7%), while others failed to show a response to IFN therapy. Overall, the factors associated with sustained antiviral effects were HCV-RNA load, HCV genotype, serum leptin level, and stage of liver fibrosi sevaluated by univariate analysis. MB was not associatedwith any therapeutic effect of IFN. Multivariate analysisindicated that HCV-RNA load was a significant risk factor, but among the patients with low viremia (HCV-RNA <100 MU / L), leptin level was an independent risk factor for IFN resistance. Namely, a high level of serum leptin attenuated the effect of IFN on both male and femalepatients with low viremia. CONCLUSION: High serum leptin level is a negative predictor of response to antiviral treatment in chronic hepatitis C with low viremia.