Oncotarget

Research Papers:

Effect of hepatic steatosis on the progression of chronic hepatitis B: A prospective cohort and in vitro study

Yangqin Chen, Chunlei Fan, Yuhan Chen, Hui Liu, Shanshan Wang, Peiling Dong, Lei Li and Huiguo Ding _

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Oncotarget. 2017; 8:58601-58610. https://doi.org/10.18632/oncotarget.17380

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Abstract

Yangqin Chen1,*, Chunlei Fan1,*, Yuhan Chen1, Hui Liu2, Shanshan Wang1,3, Peiling Dong1, Lei Li1 and Huiguo Ding1

1Department of Gastroenterology and Hepatology, Beijing You’an Hospital Affiliated with Capital Medical University, Beijing 100069, China

2Department of Pathology, Beijing You’an Hospital Affiliated with Capital Medical University, Beijing 100069, China

3Beijing Institute of Hepatology, Beijing 100069, China

*Co-first authors

Correspondence to:

Huiguo Ding, email: dinghuiguo@medmail.com.cn

Keywords: hepatic steatosis, chronic hepatitis B, hepatocellular carcinoma cells

Received: December 15, 2016    Accepted: March 22, 2017    Published: April 24, 2017

ABSTRACT

Aim: To characterize the effect of hepatic steatosis (HS) on the progression of chronic hepatitis B.

Methods: A total of 162 chronic hepatitis B (CHB) patients confirmed by liver biopsy were involved in this study. All subjects were prospectively followed-up for 5 years in real-life clinical practice. Fibrosis stage was determined using aspartate aminotransferase-to-platelet ratio index (APRI). The end-point was cirrhosis, liver cancer or death. The effects of steatosis on the biological behavior of hepatocellular carcinoma cells were investigated using oleic acid-induced lipid accumulation in HepG2, HLE, PLC, and SMMC-7721 cells.

Results: Mean age, body mass index, and serum cholesterol were significantly higher in CHB patients with HS than those without HS at baseline (p< 0.05). The APRI was lower in patients without HS at baseline (p<0.05). Compared to patients with HS, APRI of patients without HS decreased significantly during the follow-up period (p<0.05). The 5-year cumulative incidence of cirrhosis were 4.17% and 5.19% in patients without and with HS, respectively (p>0.05). The multivariate analysis showed that older (RR 1.07, 95% CI 0.996-1.149, p = 0.065) and S3 stage of liver fibrosis (RR 3.50, 95% CI 0.812–15.117, p=0.093) were risk factors for the progression to cirrhosis. In vitro, cell steatosis promoted proliferation and migration of HCC cells and conferred cell cycle at S phase.

Conclusion: The older and S3 stage of fibrosis may be risk factors for progression to cirrhosis in CHB patients with HS. HS may aggravate liver disease, promoting HCC progression.


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