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Dig Dis Sci. 2014 Oct;59(10):2571-9. doi: 10.1007/s10620-014-3180-9. Epub 2014 May 18.

Hepatic steatosis is highly prevalent in hepatitis B patients and negatively associated with virological factors.

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Department of Gastroenterology, Xinhua Hospital, Shanghai Key Laboratory of Children's Digestion and Nutrition, Shanghai Jiao Tong University School of Medicine, Shanghai, 200092, China.



The interaction between hepatitis B virus (HBV) infection and hepatic steatosis remains unclear. We aimed to explore the trend of prevalence of hepatic steatosis and its relationship with virological factors in HBV infected patients.


Consecutive untreated patients with chronic HBV infection at Shunde Hospital between 2002 and 2011 were included. Quantification of HBV replication markers was performed by enzyme immunoassay, real-time polymerase chain reaction assay and immunohistochemical staining. Hepatic steatosis was defined as at least 5% hepatocytes affected.


A total of 3,212 patients (2,574 men) with a mean age of 32 ± 9.3 years were analyzed. Serological testing showed detectable HBsAg in all, HBeAg in 63.8% and HBV DNA in 78.4% of patients. Liver biopsies demonstrated HBsAg- and HBcAg-positive immunostaining in 96.6 and 71% patients, respectively. Hepatic steatosis was present in 554 (17.3%) patients, with annual prevalence increased over time from 8.2 to 31.8% (trend analysis, x (2) = 51.657, P < 0.001). Compared to patients without steatosis, the percentages of serum HBeAg-positive and detectable HBV DNA, and intrahepatic HBsAg- and HBcAg-positive staining were decreased in steatosis patients (all P < 0.001). Adjusted for age and gender, intrahepatic HBsAg-positive staining remained as an independent factor associated with lower risk of steatosis (adjusted odds ratio 0.90, 95% confidence interval 0.835, 0.971) in multivariate analysis.


Hepatic steatosis in HBV infected patients has been raging over the past decade, and it is negatively associated with intrahepatic expression of HBsAg. Lifestyle intervention may be needed to halt the onset of steatosis in chronic HBV infection.

[Indexed for MEDLINE]

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