Factors Affecting an Increase in Spleen Volume and Association of Spleen Volume Variation with the Clinical Outcomes of Atezolizumab and Bevacizumab Treatment for Hepatocellular Carcinoma: A Retrospective Analysis.

IF 2.5 3区 医学 Q3 ONCOLOGY Oncology Pub Date : 2024-08-20 DOI:10.1159/000541002
Takeshi Hatanaka, Naoto Saito, Satoru Kakizaki, Atsushi Hiraoka, Toshifumi Tada, Kazuya Kariyama, Joji Tani, Koichi Takaguchi, Ei Itobayashi, Toru Ishikawa, Hidenori Toyoda, Kazuhito Kawata, Atsushi Naganuma, Yutaka Yata, Hideko Ohama, Tomomitsu Matono, Fujimasa Tada, Kazuhiro Nouso, Asahiro Morishita, Akemi Tsutsui, Takuya Nagano, Shinichiro Nakamura, Takashi Kumada
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引用次数: 0

Abstract

Introduction: Gastrointestinal varices rupture is considered to be prone to occur during atezolizumab and bevacizumab (Atez/Bev) treatment. This study aimed to investigate predictive factors affecting the increase in spleen volume (SpV) and the association of SpV variation with the clinical outcomes of Atez/Bev.

Methods: A total of 164 HCC patients were included in this retrospective multicenter study. We measured SpV based on CT scans obtained before treatment and at evaluations. We used the inverse probability of treatment weight to address the imbalance between patient characteristics.

Results: The median pretreatment SpV was 184 (130-257) cm3 and the median SpV variation was 27 (9-60) cm3. An increase in the SpV was observed in 140 patients (85.4%). Age <74 years (p = 0.03), mALBI grade 2b or 3 (p = 0.03), and pretreatment SpV ≥184 cm3 (p < 0.001) were significantly associated with increased SpV. There were no significant differences in progression-free survival (PFS) or overall survival (OS) between patients with SpV variation <25 cm3 and those with SpV variation ≥25 cm3 in the crude (p = 0.3 and 0.7) and IPTW-weighted cohorts (p = 0.08 and 0.8, respectively). Regarding pretreatment SpV, there were no significant differences in PFS or OS between patients with and without pretreatment spleen enlargement in the crude (both p = 0.3) and IPTW-weighted cohort (p = 0.6 and 0.3, respectively).

Conclusion: Caution is warranted to detect the aggravation of portal hypertension when administering Atez/Bev to young patients or patients with an impaired liver function or pretreatment spleen enlargement. The impact of spleen modulation by Atez/Bev appears to be limited on clinical efficacy.

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影响脾脏体积增大的因素以及脾脏体积变化与阿特珠单抗和贝伐珠单抗治疗肝细胞癌临床疗效的关系:一项回顾性分析。
简介阿特珠单抗和贝伐单抗(Atez/Bev)治疗期间容易发生消化道静脉曲张破裂。本研究旨在探讨影响脾脏体积(SpV)增加的预测因素,以及SpV变化与Atez/Bev临床结果的关联:这项回顾性多中心研究共纳入了 164 例 HCC 患者。我们根据治疗前和评估时获得的 CT 扫描结果测量了 SpV。我们使用治疗权重的逆概率来解决患者特征之间的不平衡:治疗前 SpV 的中位数为 184 (130-257) cm3,SpV 变化的中位数为 27 (9-60) cm3。140名患者(85.4%)的SpV有所增加。年龄 74 岁(p = 0.03)、mALBI 2b 或 3 级(p = 0.03)和治疗前 SpV ≥184 cm3(p <0.001)与 SpV 增加显著相关。在粗略队列(p=0.3和0.7)和IPTW加权队列(p=0.08和0.8)中,SpV变化<25 cm3的患者与SpV变化≥25 cm3的患者在无进展生存期(PFS)或总生存期(OS)方面无明显差异。关于治疗前脾脏肿大,粗略队列(p=0.3)和IPTW加权队列(p=0.6和0.3)中治疗前有脾脏肿大和没有脾脏肿大的患者的PFS或OS没有显著差异:结论:在对年轻患者或肝功能受损或治疗前脾脏肿大的患者使用 Atez/Bev 时,应谨慎检测门脉高压的加重情况。Atez/Bev对脾脏的调节对临床疗效的影响似乎有限。
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来源期刊
Oncology
Oncology 医学-肿瘤学
CiteScore
6.00
自引率
2.90%
发文量
76
审稿时长
6-12 weeks
期刊介绍: Although laboratory and clinical cancer research need to be closely linked, observations at the basic level often remain removed from medical applications. This journal works to accelerate the translation of experimental results into the clinic, and back again into the laboratory for further investigation. The fundamental purpose of this effort is to advance clinically-relevant knowledge of cancer, and improve the outcome of prevention, diagnosis and treatment of malignant disease. The journal publishes significant clinical studies from cancer programs around the world, along with important translational laboratory findings, mini-reviews (invited and submitted) and in-depth discussions of evolving and controversial topics in the oncology arena. A unique feature of the journal is a new section which focuses on rapid peer-review and subsequent publication of short reports of phase 1 and phase 2 clinical cancer trials, with a goal of insuring that high-quality clinical cancer research quickly enters the public domain, regardless of the trial’s ultimate conclusions regarding efficacy or toxicity.
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