4.3 Article

Interaction between hepatitis B virus infection and the efficacy of camrelizumab in combination with apatinib therapy in patients with hepatocellular carcinoma: a multicenter retrospective cohort study

Journal

ANNALS OF TRANSLATIONAL MEDICINE
Volume 9, Issue 18, Pages -

Publisher

AME PUBLISHING COMPANY
DOI: 10.21037/atm-21-3020

Keywords

Hepatocellular carcinoma (HCC); hepatitis B virus (HBV); camrelizumab; apatinib; reactivation

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The study explored the effects of HBV load and antiviral therapy on anti-PD-1+ antiangiogenic therapy for HCC patients. Baseline HBV loads did not affect tumor responses, and continuous effective antiviral treatment can prevent HBV reactivation.
Background: The interaction between hepatitis B virus (HBV) load and anti-programmed cell death (PD)-1 in combination with (+) antiangiogenic therapy remains controversial, especially for hepatocellular carcinoma (HCC) patients. This study sought to explore the effects of HBV load and antiviral therapy on anti-PD-1+ antiangiogenic therapy, and the rate of HBV reactivation during anti-PD-1+ antiangiogenic treatment. Methods: We performed a multicenter retrospective cohort study of camrelizumab combined with apatinib (C+A) therapy between January 1, 2019 and January 1, 2021 in patients with unresectable HCC who were seropositive for hepatitis B surface antigen (HBsAg) and received antiviral therapy before C+A involvement. The effects of HBV load and antiviral therapy on C+A and the rate of HBV reactivation during C+A treatment were examined. Results: Eighty-six patients were included in the analysis. The patients had a mean age of 55 years, and 72 (83.7%) were male. The objective response rates (ORRs) in patients with low (<2,000 IU/mL) and high (>= 2,000 IU/mL) baseline HBV deoxyribonucleic acid (DNA) levels were 34.5% and 32.2%, respectively (chi 2=0.046; P=0.829), while the disease control rates (DCRs) were 67.3% and 80.6%, respectively (chi 2=1.762; P=0.184). The results of the univariate and multivariate analyses showed that the baseline HBV DNA level did not affect PD. Additionally, none of the 86 patients suffered from HBV reactivation or HBV-related hepatic impairment with continuous antiviral treatment, regardless of nucleos(t)ide analogue (NA) type (F=1.473; P=0.228). Conclusions: Baseline HBV loads did not affect the tumor responses of HCC patients receiving anti-PD-1+ antiangiogenic therapy. Thus, HBV reactivation should not be a contradiction for anti-PD-1+ antiangiogenic therapy among patients undergoing continuous and effective antiviral treatment.

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