Effect of Metabolic Dysfunction-Associated Fatty Liver Disease on Liver Cancer Risk in a Population with Chronic HBV: A Nationwide Study

Hepatol Res. 2022 Aug 17. doi: 10.1111/hepr.13830. Online ahead of print.


BACKGROUND & AIMS: The association between metabolic dysfunction-associated fatty liver disease (MAFLD) and hepatocellular carcinoma (HCC) lacks clinical validation in at-risk populations. We assessed this relationship among chronic hepatitis B (CHB) patients.

METHODS: Data was collected from the National Health Insurance System database in South Korea. CHB patients aged over 40 years receiving health examinations between 2011 and 2012 were recruited. The primary outcome was HCC. MAFLD was defined as hepatic steatosis in combination with at least one of the following: 1) overweight, 2) diabetes, or 3) lean/normal weight with ≥2 metabolic components. Multivariable Cox-regression analysis was used to estimate adjusted hazard ratios (aHRs).

RESULTS: Of 197,346 participants, 66,149 had MAFLD; 19149, 44475, and 2,525 fulfilled diabetes (regardless of overweight), overweight alone, and lean/normal weight with ≥2 metabolic components, respectively. During follow-up (median 7 years), 13,771 developed HCC. MAFLD was independently associated with increased risk of HCC, with aHR of 1.36 (p<0.001). Propensity-score matching confirmed the same phenomena, with aHR of 1.37 (p<0.001). Furthermore, when stratified by liver cirrhosis and/or antiviral therapy, independent significances of MAFLD for HCC risk were maintained (all p<0.001). Compared with persistent non-MAFLD subgroup during entire follow-up, diagnosis of MAFLD from at least one health examinations significantly increased HCC risk with aHRs of 1.41, 1.37, and 1.14 among subgroups with persistent MAFLD, MAFLD to non-MAFLD, and non-MAFLD to MAFLD, respectively (all p<0.05).

CONCLUSIONS: MAFLD consistently increases HCC risk among CHB patients. Further studies are needed to develop an effective preventive strategy through control of metabolic health. This article is protected by copyright. All rights reserved.

PMID:35976670 | DOI:10.1111/hepr.13830

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