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Association of Serum Adipocytokines with Hepatic Steatosis and Fibrosis in Patients with Chronic Hepatitis C

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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

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