HBV Infection Linked to Threefold Increase in Fibrosis in Patients with Liver Disease


A recent study suggests that metabolic factors such as hypertension and diabetes were associated with an increased risk of liver fibrosis among patients with metabolic associated fatty liver disease who had hepatitis B virus infection.

Hepatitis B virus infection was associated with a greater risk of significant liver fibrosis in patients with metabolic associated fatty liver disease, according to a new study in China.

The study, published in Nature’s Scientific Reports, included 401 patients with metabolic associated fatty liver disease, including 179 with hepattis B virus infection (MAFLD + HBV) and 222 without HBV infection (MAFLD). They were identified between 2011 and 2021 at the Affiliated Hospital of Hangzhou Normal University in Hangzhou, China.

Patients included in the study were overweight or obese, had type 2 diabetes mellitus or had at least two metabolic risk abnormalities. The average age was 43.

“The current results indicate that the presence of HBV is associated with lower steatosis scores and ballooning grades but a higher liver fibrosis stage in patients with MAFLD,” the study authors, led by Haifeng Lv, of the First Affiliated Hospital, Zhejiang University School of Medicine, wrote. “Further risk factor analysis for liver fibrosis revealed that T2DM, hypertension, and elevated GGT levels were independent risk factors for liver fibrosis in MAFLD patients with HBV infection.”

After adjusting for confounders, HBV infection was associated with lower hepatic steatosis scores (odds ratio: 0.251, 95% confidence interval: 0.117–0.542, P < 0.001) and lower ballooning scores (OR: 0.119, 95% CI: 0.049–0.294, P < 0.001) in patients with MAFLD. But significant liver fibrosis was about triple in the MAFLD + HBV group (OR: 3.140, 95% CI: 1.479–6.663, P = 0.003).

“In our study, HBV infection resulted in a threefold increase in the risk of significant liver fibrosis in patients with MAFLD,” the authors wrote. “Therefore, for MAFLD patients with HBV infection, early screening and intervention for risk factors of liver fibrosis are required, as liver fibrosis has been identified as an accelerator for cirrhosis and hepatocellular carcinoma in chronic liver disease.”

The study also examined the risk factors for fibrosis, confirming that type 2 diabetes mellitus, hypertention and elevated gamma-glutamyl-transferase (GGT) levels were independent risk factors, with odds ratios of 4.939, 2.640 and 3.980 respectively.

“The presence of both viral and metabolic factors may accelerate disease progression in MAFLD patients with HBV infection,” the authors noted, adding that metabolic factors are more associated with liver fibrosis compared with viral factors.

Limitations of the study include that it is retrospective, it may have missed some lean or normal-weight patients with MAFLD and it couldn’t establish a causal relationship. More research is needed to better understand the effects of metabolic and viral factors on liver fibrosis in MAFLD patients with HBV infection.

“These results highlight that in addition to traditional antiviral therapy, screening and early intervention of metabolic diseases are required for MAFLD patients with HBV infection,” the authors wrote. “For patients with diabetes and hypertension, blood noninvasive biomarkers or transient elastography should be actively performed to further define the stage of liver fibrosis. If noninvasive screening presents a high risk of liver fibrosis, liver biopsy is recommended.”

Viral infections such as hepatitis and HIV have long been associated with fatty liver disease.

A recent study found that treating hepatitis C virus infection was associated with reduced liver disease burden and mortality among people who inject drugs. Other research has shown that nonalcoholic fatty liver disease is more prevalent among people living with HIV than the general population.

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