阿特唑单抗加贝伐单抗治疗与不可切除肝细胞癌患者肌肉体积损失的关系:多中心分析

IF 11.6 1区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Liver Cancer Pub Date : 2023-08-01 DOI:10.1159/000527402

Atsushi Hiraoka, Takashi Kumada, Toshifumi Tada, Masashi Hirooka, Kazuya Kariyama, Joji Tani, Masanori Atsukawa, Koichi Takaguchi, Ei Itobayashi, Shinya Fukunishi, Kunihiko Tsuji, Toru Ishikawa, Kazuto Tajiri, Hironori Ochi, Satoshi Yasuda, Hidenori Toyoda, Chikara Ogawa, Takashi Nishimura, Takeshi Hatanaka, Satoru Kakizaki, Noritomo Shimada, Kazuhito Kawata, Atsushi Naganuma, Masaki Kaibori, Takaaki Tanaka, Hideko Ohama, Kazuhiro Nouso, Asahiro Morishita, Akemi Tsutsui, Takuya Nagano, Norio Itokawa, Tomomi Okubo, Taeang Arai, Michitaka Imai, Yohei Koizumi, Shinichiro Nakamura, Kouji Joko, Hiroko Iijima, Hisashi Kosaka, Yoichi Hiasa, Masatoshi Kudo

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引用次数: 3

摘要

背景/目的:在不可切除的肝细胞癌(u-HCC)患者中，atezolizumab加贝伐单抗(Atez/Bev)治疗与肌肉体积损失(MVL)的关系尚无已知的报道。本研究旨在阐明MVL与Atez/Bev的临床关系。材料/方法:从2020年9月至2021年12月，229例u-HCC患者接受Atez/Bev治疗，并在基线时通过计算机断层扫描获得肌肉体积数据(中位年龄，74岁;男性186人(81.2%);Ecog ps 0/ 1,221 (96.5%);HCV:HBV:酒精:其他= 81:33:40:75;Child-Pugh A, 212 (92.6%);改性白蛋白-胆红素(mALBI)分级1:2a:2b = 79:60:90;BCLC 0: a: b: c = 1:24:87:117;中位观察期为6.8个月)。采用日本肝病学会的标准定义MVL，并对预后因素进行回顾性评估。结果:多因素Cox-hazard分析无进展生存期(PFS)预后因素显示，甲胎蛋白(AFP)升高(≥100 ng/mL) (HR 1.848, 95% CI 1.264-2.702, p = 0.002)、mALBI分级(≥2a) (HR 1.563, 95% CI 1.035-2.359, p = 0.034)和MVL (HR 1.479, 95% CI 1.020-2.144, p = 0.039)为显著因素。对于总生存率(OS)，显著因素包括AFP升高(≥100 ng/mL) (HR 3.564, 95% CI 1.856-6.844, p < 0.001)、mALBI分级(≥2a) (HR 3.451, 95% CI 1.580-7.538, p = 0.002)和MVL (HR 2.119, 95% CI 1.150-3.904, p = 0.016)。MVL患者(MVL组，n = 91)的PFS较无MVL患者(非MVL组，n = 138)差(中位PFS 5.3 vs. 7.6个月，p = 0.025)，而MVL组的OS较差(p = 0.038)，但均未达到中位生存时间。结论:MVL可能是u-HCC患者接受Atez/Bev治疗预后不良的一个临床因素。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

Relationship of Atezolizumab plus Bevacizumab Treatment with Muscle Volume Loss in Unresectable Hepatocellular Carcinoma Patients: Multicenter Analysis.

查看原文本刊更多论文

Relationship of Atezolizumab plus Bevacizumab Treatment with Muscle Volume Loss in Unresectable Hepatocellular Carcinoma Patients: Multicenter Analysis.

Background/aim: There is no known report regarding the relationship of atezolizumab plus bevacizumab (Atez/Bev) treatment with muscle volume loss (MVL) in unresectable hepatocellular carcinoma (u-HCC) patients. This study aimed to elucidate the clinical relationship between MVL and Atez/Bev.

Materials/methods: From September 2020 to December 2021, 229 u-HCC patients treated with Atez/Bev and with muscle volume data obtained by computed tomography at the baseline available were analyzed (median age, 74 years; males, 186 (81.2%); ECOG PS 0/1, 221 (96.5%); HCV:HBV:alcohol:others = 81:33:40:75; Child-Pugh A, 212 (92.6%); modified albumin-bilirubin (mALBI) grade 1:2a:2b = 79:60:90; BCLC 0:A:B:C = 1:24:87:117; median observation period, 6.8 months). Japan Society of Hepatology criteria were used for definition of MVL and prognostic factors were retrospectively evaluated.

Results: Multivariate Cox-hazard analysis of prognostic factors for progression-free survival (PFS) showed elevated alpha-fetoprotein (AFP) (≥100 ng/mL) (HR 1.848, 95% CI 1.264-2.702, p = 0.002), mALBI grade (≥2a) (HR 1.563, 95% CI 1.035-2.359, p = 0.034), and MVL (HR 1.479, 95% CI 1.020-2.144, p = 0.039) as significant factors. For overall survival (OS), significant factors included elevated AFP (≥100 ng/mL) (HR 3.564, 95% CI 1.856-6.844, p < 0.001), mALBI grade (≥2a) (HR 3.451, 95% CI 1.580-7.538, p = 0.002), and MVL (HR 2.119, 95% CI 1.150-3.904, p = 0.016). Patients with MVL (MVL group, n = 91) showed worse PFS than those without (non-MVL group, n = 138) (median PFS 5.3 vs. 7.6 months, p = 0.025), while the MVL group showed worse OS (p = 0.038), though neither reached the median survival time.

Conclusion: MVL may be a clinical factor related to poor prognosis in patients receiving Atez/Bev treatment for u-HCC.

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来源期刊

Liver Cancer Medicine-Oncology

CiteScore

20.80

自引率

7.20%

发文量

审稿时长

16 weeks

期刊介绍： Liver Cancer is a journal that serves the international community of researchers and clinicians by providing a platform for research results related to the causes, mechanisms, and therapy of liver cancer. It focuses on molecular carcinogenesis, prevention, surveillance, diagnosis, and treatment, including molecular targeted therapy. The journal publishes clinical and translational research in the field of liver cancer in both humans and experimental models. It publishes original and review articles and has an Impact Factor of 13.8. The journal is indexed and abstracted in various platforms including PubMed, PubMed Central, Web of Science, Science Citation Index, Science Citation Index Expanded, Google Scholar, DOAJ, Chemical Abstracts Service, Scopus, Embase, Pathway Studio, and WorldCat.