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High blood glucose marks greater liver risk when hepatitis B and fatty liver coexist

Journal of Clinical Hepatology

What is it about?

Chronic hepatitis B and steatotic liver disease can occur together, exposing the liver to both viral and metabolic injury. This study investigated whether high blood glucose adds to the risk of advanced fibrosis and end-stage liver disease in people with both conditions.

Researchers established a retrospective cohort of 668 adults whose liver disease had been confirmed by biopsy. High blood glucose was defined as fasting glucose of at least 6.1 mmol/L or a diagnosis of type 2 diabetes. After matching patients to balance baseline differences, the analysis compared 82 people with hyperglycaemia and 281 without it.

Patients with hyperglycaemia had more metabolic abnormalities, more severe fat accumulation in the liver and a higher prevalence of advanced fibrosis. After adjustment for other factors, hyperglycaemia was associated with 1.75 times the odds of advanced fibrosis.

The cohort was followed for outcomes including decompensated cirrhosis, liver cancer, transplantation and liver-related death. Among patients who already had advanced fibrosis, hyperglycaemia was associated with approximately 3.2 times the risk of developing end-stage liver disease.

These results indicate that glucose abnormalities may help identify a particularly vulnerable subgroup among patients affected by both hepatitis B and fatty liver disease.

Why is it important?

Clinical management of chronic hepatitis B often focuses on suppressing the virus, but metabolic factors may continue to drive liver damage. When fatty liver and hyperglycaemia are also present, controlling viral replication alone may not address the full risk.

The study supports regular assessment of blood glucose in people with combined hepatitis B and steatotic liver disease, particularly when advanced fibrosis is already present. It also suggests that metabolic management should form part of long-term liver care.

Nevertheless, this was an observational study and cannot prove that lowering glucose will prevent fibrosis or end-stage disease. The number of outcome events was limited, as reflected by the wide confidence interval. Prospective studies should test whether glucose control improves liver outcomes.

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