Abstract
Aims: A high baseline hepatitis B virus (HBV) load has always
been listed as an exclusion criterion for programmed cell death-1 (PD-1)
inhibitor-associated therapy in clinical trials, as the interaction
between HBV load and anti-PD-1/PD-L1 therapy remains controversial.
Methods: We performed a retrospective cohort study of
unresectable HCC patients who were seropositive for HBsAg and accepted
tenofovir alafenamide fumarate (TAF) therapy before anti-PD-1 in
combination with an antiangiogenic treatment. Patients were divided into
a low HBV DNA group (≤ 2000 IU/ml) and a high HBV DNA group
(> 2000 IU/ml) according to the baseline HBV DNA levels.
Tumour response and progression-free survival (PFS) were compared, and
univariate and multivariate Cox analyses were performed to identify
potential risk factors for PFS. The incidences of HBV reactivation and
HBV-associated hepatitis were also recorded.
Results: Seventy eligible patients were included: 48 in the low
group and 22 in the high group. The objective response rates (ORRs),
disease control rates (DCRs), and PFS did not differ significantly
between the two groups (P = 0.761, 0.552, and 0.784,
respectively). The results of Cox analyses revealed that the baseline
HBV load did not affect PFS. Additionally, HBV reactivation occurred in
only 2 patients (2.9%), and no patient experienced HBV-related hepatic
impairment when given a continuous TAF treatment.
Conclusions: Baseline HBV loads do not affect the prognosis of
HCC patients receiving anti-PD-1 in combination with an antiangiogenic
therapy, while PD-1 inhibitors do not aggravate HBV reactivation and
hepatic impairment in patients simultaneously subjected to TAF
prophylaxis.