ArticleHeliyon2024
Chronic hepatitis B and metabolic dysfunction-associated steatotic liver disease: Metabolic risk factors are key drivers of hepatocellular carcinoma.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Comparison of patients with HCC with and without MASLD after surgical resection.JHEP reports : innovation in hepatology · 2026Article
- Observational
- Article
- Review
- Development and Validation of a Predictive Nomogram for Myelosuppression Risk in Chronic Hepatitis B Patients Treated with Peginterferon.Infection and drug resistance · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Chronic hepatitis B (CHB) and metabolic dysfunction-associated steatotic liver disease (MASLD) are the leading causes of hepatocellular carcinoma (HCC). This study aimed to explore the impact of baseline MASLD on the risk of HCC development in patients with CHB receiving antiviral treatment. Methods: We consecutively recruited 535 patients with CHB who initiated antiviral treatment between January 2007 and January 2023. The exclusion criteria included coexisting HDV, HCV, or HIV infection; other chronic liver diseases; extrahepatic malignancies; prior HCC; and HCC development within one year. A baseline liver biopsy was performed in 467 patients (87 %). MASLD was defined as hepatic steatosis diagnosed histologically or by imaging, combined with one cardiometabolic risk factor. The cumulative incidence of HCC and its associated factors was analyzed in patients with CHB, with and without MASLD. Results: In total, 535 treatment-naïve patients with CHB were included, with a median follow-up of 6.05 years. MASLD was not associated with an increased incidence of HCC in patients with CHB (HR: 1.17; 95 % CI: 0.77-1.79; p = 0.466). The cumulative incidence of HCC increased with the number of fulfilled cardiometabolic criteria (0-2 criteria vs. ≥ 3 criteria) (HR: 3.93; 95 % CI: 1.89-8.19; p < 0.001).Age (HR: 1.03, 95 % CI 1.01-1.06, p = 0.010), male sex (HR: 3.17; 95 % CI 1.34-7.53, p = 0.009), diabetes (HR: 2.81; 95 % CI 1.54-5.12, p < 0.001), and cirrhosis (HR:3.03; 95 % CI 1.57-5.5.86, p < 0.001) were independently associated with HCC development. Conclusions: It was not MASLD, but rather the presence of multiple cardiometabolic risk factors in patients with CHB that was associated with the risk of HCC in those receiving antiviral treatment. Furthermore, older age, male sex, diabetes, and cirrhosis aggravated the risk of HCC in patients with CHB.
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