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. 2022 Oct 26;14(11):2355.
doi: 10.3390/v14112355.

Application and Impact of Antiviral Therapy for Patients with HBV-Related Hepatocellular Carcinoma Receiving Sorafenib and Lenvatinib Treatment

I-Cheng Lee  1   2 , Pei-Chang Lee  1   2 , Yee Chao  2   3 , Chen-Ta Chi  1   2   4 , Chi-Jung Wu  1   2   4 , Yi-Ping Hung  2   3 , Chien-Wei Su  1   2 , Ming-Chih Hou  1   2 , Yi-Hsiang Huang  1   2   4
Affiliations

Application and Impact of Antiviral Therapy for Patients with HBV-Related Hepatocellular Carcinoma Receiving Sorafenib and Lenvatinib Treatment

I-Cheng Lee et al. Viruses. .

Abstract

Overall survival (OS) in patients with advanced hepatocellular carcinoma (HCC) has improved in the era of multi-line sequential therapy. The application of antiviral therapy and its impact on survival for patients with HBV-related HCC needs to be reassessed. The aim of this study was to evaluate the application and impact of antiviral therapy on survival for patients with HBV-related HCC receiving tyrosine kinase inhibitor (TKI) therapy. Patients with advanced HBV-related HCC treated with sorafenib or lenvatinib as first-line therapy with (n = 377) and without (n = 182) nucleos(t)ide analogue (NUC) therapy were retrospectively enrolled. Prognostic factors of OS were evaluated. Secular trends in the increased application of NUC therapy and improved survival were observed in the last decade. The HBV reactivation rate in patients without NUC therapy was 6.6%. By multivariate analysis, baseline low HBV viral load, achieving undetectable HBV DNA after TKI therapy, and ability to receive second-line therapy were found to be independent predictors of OS. In subgroup patients with NUC therapy, starting NUC before TKI was associated with a better OS. In conclusion, the application of antiviral therapy for patients with HBV-related HCC receiving TKI therapy has increased over time. Achieving complete virological suppression may contribute to a better OS in patients with advanced HBV-related HCC.

Keywords: antiviral therapy; entecavir; hepatitis B virus; hepatocellular carcinoma; lenvatinib; sorafenib; tenofovir; tyrosine kinase inhibitor.

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Conflict of interest statement

Y.-H.H. has received research grants from Gilead Sciences and Bristol-Meyers Squibb, and honoraria from Abbvie, Gilead Sciences, Bristol-Meyers Squibb, Ono Pharmaceutical, Merck Sharp & Dohme, Eisai, Eli Lilly, Ipsen, and Roche and has served in an advisory role for Abbvie, Gilead Sciences, Bristol-Meyers Squibb, Ono Pharmaceuticals, Eisai, Eli Lilly, Ipsen, Merck Sharp & Dohme, and Roche. I.-C.L. has received honoraria from Gilead Sciences, Bristol-Meyers Squibb, Abbvie, Merck Sharp & Dohme, Bayer, Eisai, Ipsen, and Roche and has served in an advisory role for Gilead Sciences. The other authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Screening, enrollment, and grouping of patients.
Figure 2
Figure 2
Secular trends in overall survival (OS) and nucleos(t)ide analogue (NUC) therapy uptake from 2012 to 2022. (A) Secular trends in OS from 2012 to 2022. (B) Proportion of patients receiving NUC therapy and second-line systemic therapy from 2012 to 2022. (C) Progression-free survival (PFS) in patients receiving lenvatinib or sorafenib from 2019 to 2022. (D) OS in patients receiving lenvatinib or sorafenib during 2019–2022.
Figure 3
Figure 3
Kaplan–Meier curves of overall survival (OS) in patients with HBV-related HCC. (A) OS in patients with and without nucleos(t)ide analogue (NUC) therapy. (B) OS stratified by HBV DNA level. (C) OS in patients with and without achieving undetectable HBV DNA. (D) OS in patients with and without second-line (2L) therapy. (E) OS in subgroup patients with NUC therapy who started NUC before and after TKI treatment. (F) OS in subgroup patients with NUC therapy with and without achieving undetectable HBV DNA.
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