ReviewClinical and molecular hepatology2026
Chronic viral hepatitis with concurrent metabolic dysfunction-associated steatotic liver disease: dual etiology challenges.
Review in Clinical and molecular hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Steatotic liver disease spectrum: From MASLD to MetALD and beyond - Clinical outcomes and precision medicine frontiers.Clinical and molecular hepatology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The overlapping epidemics of chronic viral hepatitis and metabolic dysfunction-associated steatotic liver disease (MASLD) present a complex challenge in modern hepatology. In chronic hepatitis B, a unique "steatosis paradox" emerges: while isolated hepatic steatosis provides a suppressive microenvironment that promotes hepatitis B viral clearance, the concomitant systemic cardiometabolic burden acts dose-dependently to drive fibrogenesis and hepatocellular carcinoma (HCC). Conversely, chronic hepatitis C and host metabolic dysfunctions exhibit synergistic destruction. Hepatitis C virus actively hijacks lipid metabolism and induces insulin resistance. Even after viral eradication via direct-acting antivirals, residual steatosis and glycemic abnormalities remain formidable drivers of HCC. Consequently, the traditional virocentric paradigm is no longer sufficient. Clinical management should pivot toward precision risk stratification and a multidisciplinary dual-target approach, equally prioritizing sustained viral suppression and aggressive metabolic remission. This review summarizes the divergent virus-MASLD interactions, optimal clinical strategies, current challenges and future opportunities.
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