Journal of Gastroenterology and Hepatology
Published Online: 30 Jul 2010
Journal compilation © 2010 Blackwell Publishing Asia Pty Ltd and Journal of Gastroenterology and Hepatology Foundation
Jee-Fu Huang 1-3 ; Chung-Feng Huang 2,3 ; Ming-Lung Yu 3,4 ; Chia-Yen Dai 3,4 ; Ching-I Huang 2,3 ; Ming-Lun Yeh 2,3 ; Meng-Hsuan Hsieh 5 ; Jeng-Fu Yang 6 ; Ming-Yen Hsieh 3 ; Zu-Yau Lin 3,4 ; Shinn-Chern Chen 3,4 ; Wan-Long Chuang 3,4
1 Department of Internal Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
2 Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
3 Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
4 Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
5 Department of Occupational and Environmental Medicine, Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
6 Department of Preventive Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.
Correspondence to Wan-Long Chuang M.D., Ph.D.,
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Tzyou Road, Kaohsiung City 807, Taiwan.
Tel: +886-7-3208282
Fax: +886-7-312-3955
Email:jf71218@gmail.com; waloch@cc.kmu.edu.tw
Financial and conflict of interest: none
CONTRIBUTIONS OF AUTHORS:
Conception and design: Jee-Fu Huang, Chia-Yen Dai, Ming-Lung Yu, Wan-Long Chuang, Chung-Feng Huang
Acquisition of data: Jee-Fu Huang, Chia-Yen Dai, Ming-Yen Hsieh, Chung-Feng Huang, Ching-I Huang, Ming-Lun Yeh, Zu-Yau Lin, Shinn-Chern Chen
Data analysis and interpretation: Jee-Fu Huang, Chung-Feng Huang, Chia-Yen Dai, Wan-Long Chuang, Ming-Lung Yu
Manuscript drafting and critical revising: Jee-Fu Huang, Chia-Yen Dai, Ming-Lung Yu, Wan-Long Chuang
This is an Accepted Article that has been peer-reviewed and approved for publication in the Journal of Gastroenterology and Hepatology, but has yet to undergo copy-editing and proof correction. Please cite this article as an "Accepted Article"; doi: 10.1111/j.1440-1746.2010.06438.x
KEYWORDS
hepatitis C virus • visfatin • histological activity index • fibrosis
ABSTRACT
Background & Aim: Cytokines activation is a common feature in chronic hepatitis C (CHC) infection. Visfatin, as a recently-recognized adipocytokine, may correlate with metabolic abnormalities. We aimed to elucidate the characteristics of visfatin in CHC patients.
Methods: This retrospective study included 102 treatment-naïve CHC patients and 97 sex-/age-matched healthy adults. Serum visfatin levels were examined by an ELISA test. The correlation between visfatin and hepatitis C virus (HCV) infection in terms of virological, metabolic, and histopathological profiles was analyzed. The impact of visfatin on the treatment response to pegylated interferon plus ribavirin (PEGIFN/RBV) therapy was also assessed.
Results: The visfatin level was correlated significantly with fibrosis scores (r = 0.23, P = 0.02) in CHC patients. A significant higher visfatin level was observed in CHC patients with histological activity index scores of mild and more (P = 0.01) and advanced fibrosis (P = 0.04). The mean visfatin level (0.81 ± 0.28 log ng/mL) of 26 CHC patients with metabolic syndrome was significantly lower than their counterparts (0.95 ± 0.30 log ng/mL) (P = 0.03). There was no significant correlation between visfatin and HCV genotypes, viral load, and treatment response to PEGIFN/RBV therapy. Multiple logistic regression analyses demonstrated that MS was the leading negative variable (OR = 0.09, 95% CI = 0.02–0.46, P = 0.004) associated with high visfatin level, followed by advanced fibrosis (OR = 2.88, 95% CI = 1.06–6.78, P = 0.03).
Conclusions: Serum visfatin was correlated with disease severity and metabolic syndrome in CHC patients.
Received date: 23-Jan-2010
Accepted date: 8-Jul-2010
DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1440-1746.2010.06438.x About DOI
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