Metabolic dysfunction-associated steatotic liver disease patients with advanced fibrosis face high hepatocellular carcinoma risk over ten years

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Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association Published May 2, 2026 Medically reviewed May 2, 2026 Study authors: Lim Ryan Yanzhe, Tan Faith Xin Ning, Ho Glenn Jun Kit, Tham Ethan Kai Jun, Kow Alfred, Lv Guoyue, Fa… PubMed ↗ DOI ↗ By Dr. Amelia Tan, PhD · Internal Medicine & Chronic Disease

Key Takeaway

Advanced fibrosis in metabolic dysfunction-associated steatotic liver disease drastically increases hepatocellular carcinoma risk, necessitating enhanced surveillance protocols.

This extensive meta-analysis examined nearly 4 million individuals to determine the long-term risk of developing hepatocellular carcinoma in people with metabolic dysfunction-associated steatotic liver disease. The study compared outcomes between those with known advanced fibrosis and those without, utilizing data from both administrative databases and hospital-based records.

Results indicate that the ten-year cumulative incidence of hepatocellular carcinoma varies significantly depending on fibrosis status. In administrative database studies, the risk was 8.8% for those with advanced fibrosis versus 1.3% for those without. Hospital and clinic-based studies showed even wider disparities, with incidences of 48.5% and 18.3% respectively for the two groups.

Statistical analysis confirmed a significantly higher risk of hepatocellular carcinoma in patients with advanced fibrosis compared to those without. Hazard ratios were 11.09 in administrative studies and 10.50 in hospital studies, with both showing highly significant p-values. These findings underscore the critical importance of identifying fibrosis stage for accurate risk stratification.

While selection bias may influence results in hospital-based settings, the consistency of elevated risk across study types supports the need for tailored surveillance strategies. Future research should focus on refining algorithms to better predict hepatocellular carcinoma progression in this high-risk population.

Study Details

Study typeMeta analysis

EvidenceLevel 1

Follow-up120.0 mo

PublishedMay 2026

PMID40935097

View Original Abstract ↓

BACKGROUND & AIMS: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the fastest rising etiology of hepatocellular carcinoma (HCC). The time-dependent incidence of HCC in people with MASLD has not been reported. We aimed to provide robust estimates for HCC incidence in MASLD. METHODS: Medline and Embase were searched from inception to November 2024. Individual participant data were reconstructed from published Kaplan-Meier curves, and a pooled analysis of cumulative HCC incidence from time-to-event data was performed using a random-effects model. RESULTS: We screened 4951 articles and included 26 studies (3,995,728 individuals). The 1-, 3-, 5-, and 10-year cumulative incidence of HCC in people with MASLD and known advanced fibrosis was 0.8%, 2.4%, 3.9%, and 8.8%, respectively, in administrative database studies, and 3.9%, 11.7%, 21.0% and 48.5%, respectively, in hospital/clinic-based studies. The 1-, 3-, 5-, and 10-year cumulative incidence of HCC in people with MASLD but without advanced fibrosis was 0.1%, 0.5%, 0.7%, and 1.3%, respectively, in administrative database studies, and 1.6%, 4.7%, 8.2%, and 18.3%, respectively, in hospital/clinic-based studies. Selection bias may contribute to the elevated risk in hospital/clinic-based studies. The risk of HCC in patients with advanced fibrosis was significantly higher compared with those without advanced fibrosis in both administrative database (hazard ratio [HR], 11.09; 95% confidence interval [CI], 2.68-45.89; P < .001) and hospital/clinic-based studies (HR, 10.50; 95% CI, 3.19-34.51; P < .001). CONCLUSIONS: This reconstructed individual participant data meta-analysis provides updated estimates for HCC incidence in people with MASLD. The incidence of HCC is elevated in people with MASLD and advanced fibrosis. These data may have implications for further research in HCC surveillance and future development of surveillance algorithms.