Guest guest Posted September 17, 2010 Report Share Posted September 17, 2010 http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract & ArtikelNr=\ 314592 & Ausgabe=254590 & ProduktNr=223838 Original Paper Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis C Ancha Baranovaa-c, Mohammed H. Jarrara, b, Stepanovaa, b, Nila Rafiqa, c, Terry Gramlichd, Vikas Chandhokea, b, Zobair M. Younossia-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, Mason University, Fairfax, Va., cCenter for Liver Diseases, Inova Fairfax Hospital, Falls Church, Va., and dAmeriPath, Cleveland, Ohio, USA Address of Corresponding Author Digestion 2011;83:32-40 (DOI: 10.1159/000314592) Abstract 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-á. 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. S. Karger AG, Basel Author Contacts Zobair M. Younossi, MD, MPH Center for Liver Diseases at Inova Fairfax Hospital Center for Integrated Research, Inova Health System 3300 Gallows Road, Falls Church, VA 22042 (USA) Tel. +1 703 776 2540, Fax +1 703 776 4388, E-Mail zobair.younossi@... -------------------------------------------------------------------------------- Article Information Received: February 1, 2010 Accepted: April 22, 2010 Published online: September 15, 2010 Number of Print Pages : 9 Number of Figures : 3, Number of Tables : 6, Number of References : 38 Additional supplementary material is available online - Number of Parts : 1 Original Paper Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis C Ancha Baranovaa-c, Mohammed H. Jarrara, b, Stepanovaa, b, Nila Rafiqa, c, Terry Gramlichd, Vikas Chandhokea, b, Zobair M. Younossia-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, Mason University, Fairfax, Va., cCenter for Liver Diseases, Inova Fairfax Hospital, Falls Church, Va., and dAmeriPath, Cleveland, Ohio, USA Address of Corresponding Author Digestion 2011;83:32-40 (DOI: 10.1159/000314592) Key Words Hepatitis C Visfatin Tumor necrosis factor-á Interleukin-6 Interleukin-8 Steatosis Resistin Abstract 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-á. 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. S. Karger AG, Basel Author Contacts Zobair M. Younossi, MD, MPH Center for Liver Diseases at Inova Fairfax Hospital Center for Integrated Research, Inova Health System 3300 Gallows Road, Falls Church, VA 22042 (USA) Tel. +1 703 776 2540, Fax +1 703 776 4388, E-Mail zobair.younossi@... Article Information Received: February 1, 2010 Accepted: April 22, 2010 Published online: September 15, 2010 Number of Print Pages : 9 Number of Figures : 3, Number of Tables : 6, Number of References : 38 Additional supplementary material is available online - Number of Parts : 1 Journal Home Journal Content Guidelines Editorial Board Aims and Scope Subscriptions Download Citation This journal is part of the third subject package of the Karger Journal Archive Collection Information on packages (PDF) Free sample issues For non-native English speakers and international authors who would like assistance with their writing before submission, we suggest American Journal Experts for their scientific editing service. © 2010 S. 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