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  • Title: Adiponectin: a new independent predictor of liver steatosis and response to IFN-alpha treatment in chronic hepatitis C.
    Author: Zografos TA, Liaskos C, Rigopoulou EI, Togousidis E, Makaritsis K, Germenis A, Dalekos GN.
    Journal: Am J Gastroenterol; 2008 Mar; 103(3):605-14. PubMed ID: 18190648.
    Abstract:
    OBJECTIVES: To compare serum adiponectin and tumor necrosis factor (TNF)-alpha among patients with viral liver diseases; to investigate associations of serum adiponectin and TNF-alpha with histological or viral characteristics of chronic hepatitis C (CHC); to investigate adiponectin and TNF-alpha alterations during interferon (IFN)-alpha treatment; and to assess the relationship between serum adiponectin and TNF-alpha and response rates to treatment. METHODS: Adiponectin (mug/mL) and TNF-alpha (pg/mL) determinations by enzyme-linked immunosorbent assay (ELISA) in serial samples (before, the middle, the end, and 6 months after the end of treatment) from 83 CHC and 59 chronic hepatitis B (CHB) patients. Forty-three blood donors served as healthy controls. Patients were treated with IFN-alpha (4.5 MU/t.i.w.) for 12 months in CHB cases, and IFN-alpha (3 MU/t.i.w.) plus ribavirin for 6-12 months according to hepatitis C virus (HCV) genotype in CHC cases. RESULTS: After adjustment for gender and body mass index (BMI), HCV genotype 3 overweight patients (BMI > 25 kg/m(2)) had significantly lower adiponectin (7.3 +/- 2.7) at baseline compared with non-3 HCV genotype overweight patients (P < 0.05). Lower adiponectin (HCV genotype 3, P= 0.02 and HCV genotype 1, P= 0.025) and higher TNF-alpha (P= 0.025) at baseline were identified as independent predictors of liver steatosis in CHC patients. Lower adiponectin was also identified as an independent predictor of no virological response at the end of treatment (odds ratio [OR] 0.76, 95% confidence interval [CI] 0.66-0.87, P < 0.001). At the end of IFN-alpha therapy, only HCV genotype 3 patients had significantly higher serum adiponectin (10.4 +/- 6.3) compared with its levels before treatment (8.7 +/- 4.7, P < 0.05). CONCLUSIONS: This study suggests that HCV genotype 3 may directly affect adiponectin. This is further supported by the significant increase in adiponectin at the end of treatment only in HCV genotype 3 patients. Serum adiponectin at baseline appears to be an independent predictor of liver steatosis and for the achievement of end-of-treatment virological response, while serum TNF-alpha at baseline was identified as an independent predictor only of liver steatosis.
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