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Postoperative hepatitis B virus reactivation and its impact on survival in HBV-related hepatocellular carcinoma patients undergoing conversion therapy with interventional therapy combined with tyrosine kinase inhibitors and immune checkpoint inhibitors

医学 肝细胞癌 内科学 乙型肝炎病毒 胃肠病学 比例危险模型 肿瘤科 丙型肝炎病毒 生存分析 乙型肝炎 免疫学 病毒
作者
Shiqing Xu,Qingqing Pang,Meng Wei,Danxi Liu,Yuan Du,Tao Bai,Xiaobo Wang,Zhihong Tang,Feixiang Wu
出处
期刊:Frontiers in Cellular and Infection Microbiology [Frontiers Media]
卷期号:15: 1598193-1598193 被引量:3
标识
DOI:10.3389/fcimb.2025.1598193
摘要

Objective This study aimed to investigate hepatitis B virus (HBV) reactivation and its impact on postoperative survival in patients with HBV-related hepatocellular carcinoma (HCC) who underwent conversion therapy. The therapeutic regimen consisted of interventional procedures (hepatic artery infusion chemotherapy [HAIC] and/or transarterial chemoembolization [TACE]) combined with tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs). Methods A retrospective analysis was performed at a single institution involving 91 patients who had initially unresectable HCC linked to the hepatitis B virus. These patients achieved resectability following conversion therapy and subsequently underwent surgical tumor removal. Logistic regression identified risk factors for HBV reactivation (HBVr). Kaplan-Meier survival analysis and log-rank tests assessed survival differences. Cox proportional hazards regression was used to identify independent predictors of progression-free survival (PFS) and overall survival (OS). Results In our cohort, HBVr occurred in 17 patients (18.7%), all of whom received antiviral therapy. The incidence of HBVr was 16.7% (14/84) in patients with detectable baseline HBV DNA and 42.9% (3/7) in those with undetectable levels. Baseline HBV DNA ≥2000 IU/ml was identified as an independent protective factor against HBVr (OR 0.090, 95% CI 0.015–0.532; P = 0.008). The median PFS was significantly shorter in the reactivation group than in the non-reactivation group (12.1 months [95% CI 5.5–18.7] vs . 29.2 months [95% CI 23.6–34.7]; P < 0.001). However, no significant difference was observed in median OS between the two groups (not reached vs . 45.6 months [95% CI 41.7–49.5]; P = 0.117). Conclusion HBVr represents a potential complication in subjects receiving hepatectomy for hepatitis B virus associated HCC following conversion therapy involving interventional therapies combined with TKIs and ICIs. Patients experiencing HBVr exhibited significantly shorter progression-free survival compared to those without reactivation. Therefore, prophylactic antiviral therapy and meticulous HBV DNA monitoring are warranted during both conversion therapy and the perioperative period.
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