Annals of clinical and laboratory science · 2013
The effect of hepatitis B virus infection on hepcidin expression in hepatitis B patients.
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Wang Xue-hua, Cheng Pan-Pan, Jiang Fang, Jiao Xiao-Yang
Аннотация
BACKGROUND: Hepcidin is a central regulator of iron metabolism. As hepcidin is produced mainly by hepatocytes, pathologic changes in the liver may affect hepcidin production. Abnormal hepcidin expression has been reported following liver injury, including liver cirrhosis, alcoholic liver disease, and chronic hepatitis B and hepatitis C. However, it is unclear whether there is a dose-dependent relationship between hepcidin expression and hepatitis B virus load. The aim of this study was to characterize hepcidin levels in patients with different hepatitis B virus (HBV) DNA levels.
METHODS: We investigated serum hepcidin levels in 71 patients with different HBV DNA loads, 10 patients with hepatocelluar carcinoma (HCC), and 13 healthy individuals. The relationships between hepcidin expression and hematological/liver functional parameters, iron, and inflammatory indicators were also analyzed.
RESULTS: Serum IL-6, ferritin, and hepcidin levels were significantly higher in patients with hepatitis B and in HCC patients than in controls (P<0.05), and strong positive correlations were found between hepcidin and ferritin, AST, ALT, GGT, ALP, TBIL, IBIL, and AFU, as well as between log [hepcidin] and log [HBV], respectively. There were no significant differences in hematological parameters, including WBC, Hb, and platelets among hepatitis B patients, nor was a correlation found between hepcidin and any hematological parameters.
CONCLUSION: Our results indicate that hepcidin expression is regulated by iron and inflammatory factors in hepatitis B infection patients, and that the virus load can affect hepcidin production.
METHODS: We investigated serum hepcidin levels in 71 patients with different HBV DNA loads, 10 patients with hepatocelluar carcinoma (HCC), and 13 healthy individuals. The relationships between hepcidin expression and hematological/liver functional parameters, iron, and inflammatory indicators were also analyzed.
RESULTS: Serum IL-6, ferritin, and hepcidin levels were significantly higher in patients with hepatitis B and in HCC patients than in controls (P<0.05), and strong positive correlations were found between hepcidin and ferritin, AST, ALT, GGT, ALP, TBIL, IBIL, and AFU, as well as between log [hepcidin] and log [HBV], respectively. There were no significant differences in hematological parameters, including WBC, Hb, and platelets among hepatitis B patients, nor was a correlation found between hepcidin and any hematological parameters.
CONCLUSION: Our results indicate that hepcidin expression is regulated by iron and inflammatory factors in hepatitis B infection patients, and that the virus load can affect hepcidin production.