Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis CBaranova A.a–c · Jarrar M.H.a, b · Stepanova M.a · Johnson A.b · Rafiq N.a, c · Gramlich T.d · Chandhoke V.a, b · Younossi Z.M.a–c
aTranslational Research Institute, Betty and Guy Beatty Center for Integrated Research, Inova Health System, Falls Church, Va., bMolecular and Microbiology Department and Center for the Study of Genomics in Liver Diseases, George Mason University, Fairfax, Va., cCenter for Liver Diseases, Inova Fairfax Hospital, Falls Church, Va., and dAmeriPath, Cleveland, Ohio, USA Digestion 2011;83:32–40 (DOI:10.1159/000314592)
Background: The pathogenic mechanisms of hepatic steatosis in hepatitis C (HCV) remain unclear. Aim: To assess the potential role of cytokines and adipokines in HCV-related steatosis and fibrosis. Methods: We profiled several adipokines, cytokines, and related soluble molecules in 99 HCV patients and analyzed their potential associations with hepatic steatosis and fibrosis. Results: Serum leptin and IL-1RA were significantly higher in HCV genotype 1 as compared to genotype 3. On the other hand, serum resistin, IL-8, IL-1B and sIL-6R, were significantly higher in HCV genotype 3. No differences were observed for adiponectin, visfatin, IL-6 and TNF-α. Regardless of HCV genotype, steatosis could be predicted by a combination of IL-8, IL-6, and sIL-6R/IL-6. When analysis was repeated for each of the genotypes, the reliability of models improved. Regardless of HCV genotype, moderate to severe fibrosis (Metavir score >F2), was predicted by IL-8 and resistin levels. Conclusions: Analysis of adipocytokines associated with steatosis supports the hypothesis that steatogenic pathways differ in HCV genotype 3 from those infected with non-genotype 3 infections.
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