Hyperprogressive disease in patients with unresectable hepatocellular carcinoma receiving atezolizumab plus bevacizumab therapy.

atezolizumab plus bevacizumab hepatocellular carcinoma hyperprogressive disease

Journal

Hepatology research : the official journal of the Japan Society of Hepatology
ISSN: 1386-6346
Titre abrégé: Hepatol Res
Pays: Netherlands
ID NLM: 9711801

Informations de publication

Date de publication:
Mar 2022
Historique:
revised: 18 11 2021
received: 28 09 2021
accepted: 13 12 2021
pubmed: 18 12 2021
medline: 18 12 2021
entrez: 17 12 2021
Statut: ppublish

Résumé

Atezolizumab plus bevacizumab was approved for hepatocellular carcinoma (HCC) patients in 2020, but treatment outcomes of atezolizumab plus bevacizumab in real-world settings remain unclear. Hyperprogressive disease (HPD), an acceleration of tumor growth occurring in some types of malignancies treated with immune checkpoint inhibitors, was assessed in HCC patients receiving atezolizumab plus bevacizumab. Tumor growth kinetics (TGK) and tumor growth rate (TGR) were calculated at pre- and post-treatment in 88 Japanese patients with HCC receiving atezolizumab plus bevacizumab. Hyperprogressive disease was defined as progressive disease (PD) with ≥ two-fold increase in TGK and TGR. The association of baseline characteristics with HPD was analyzed. The best objective responses were partial response, stable disease, and PD in 12 (13.6%), 51 (58.0%), and 25 (28.4%) patients, respectively. The median progression-free survival was 5.0 months. Eleven (12.5%) and 9 (10.2%) patients had a TGK ratio and a TGR ratio of ≥2, respectively. Hyperprogressive disease was observed in nine patients (10.2%) and they showed significantly shorter overall survival than patients without HPD (median, 4.3 months vs. not reached; p < 0.001). Patients with HPD had larger and more intrahepatic tumors, higher levels of α-fetoprotein and lactate dehydrogenase, and higher neutrophil-to-lymphocyte ratio (NLR) at baseline than patients without HPD. NLR of ≥3 at baseline was identified as the only independent factor associated with HPD in multivariate analysis. Hyperprogressive disease was observed in 10.2% of HCC patients receiving atezolizumab plus bevacizumab, and an elevated NLR at baseline had an increased risk of HPD.

Sections du résumé

BACKGROUND BACKGROUND
Atezolizumab plus bevacizumab was approved for hepatocellular carcinoma (HCC) patients in 2020, but treatment outcomes of atezolizumab plus bevacizumab in real-world settings remain unclear. Hyperprogressive disease (HPD), an acceleration of tumor growth occurring in some types of malignancies treated with immune checkpoint inhibitors, was assessed in HCC patients receiving atezolizumab plus bevacizumab.
METHODS METHODS
Tumor growth kinetics (TGK) and tumor growth rate (TGR) were calculated at pre- and post-treatment in 88 Japanese patients with HCC receiving atezolizumab plus bevacizumab. Hyperprogressive disease was defined as progressive disease (PD) with ≥ two-fold increase in TGK and TGR. The association of baseline characteristics with HPD was analyzed.
RESULTS RESULTS
The best objective responses were partial response, stable disease, and PD in 12 (13.6%), 51 (58.0%), and 25 (28.4%) patients, respectively. The median progression-free survival was 5.0 months. Eleven (12.5%) and 9 (10.2%) patients had a TGK ratio and a TGR ratio of ≥2, respectively. Hyperprogressive disease was observed in nine patients (10.2%) and they showed significantly shorter overall survival than patients without HPD (median, 4.3 months vs. not reached; p < 0.001). Patients with HPD had larger and more intrahepatic tumors, higher levels of α-fetoprotein and lactate dehydrogenase, and higher neutrophil-to-lymphocyte ratio (NLR) at baseline than patients without HPD. NLR of ≥3 at baseline was identified as the only independent factor associated with HPD in multivariate analysis.
CONCLUSIONS CONCLUSIONS
Hyperprogressive disease was observed in 10.2% of HCC patients receiving atezolizumab plus bevacizumab, and an elevated NLR at baseline had an increased risk of HPD.

Identifiants

pubmed: 34918428
doi: 10.1111/hepr.13741
doi:

Types de publication

Journal Article

Langues

eng

Pagination

298-307

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2021 The Japan Society of Hepatology.

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Auteurs

Kazuki Maesaka (K)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Ryotaro Sakamori (R)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Ryoko Yamada (R)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Yuki Tahata (Y)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Yasuharu Imai (Y)

Department of Gastroenterology and Hepatology, Ikeda Municipal Hospital, Ikeda, Osaka, Japan.

Kazuyoshi Ohkawa (K)

Department of Hepatobiliary and Pancreatic Oncology, Osaka International Cancer Institute, Osaka, Osaka, Japan.

Masanori Miyazaki (M)

Department of Gastroenterology and Hepatology, Osaka Police Hospital, Osaka, Osaka, Japan.

Eiji Mita (E)

Department of Gastroenterology and Hepatology, National Hospital Organization Osaka National Hospital, Osaka, Osaka, Japan.

Toshifumi Ito (T)

Department of Gastroenterology and Hepatology, Japan Community Healthcare Organization, Osaka Hospital, Osaka, Osaka, Japan.

Hideki Hagiwara (H)

Department of Gastroenterology and Hepatology, Kansai Rosai Hospital, Amagasaki, Hyogo, Japan.

Takayuki Yakushijin (T)

Department of Gastroenterology and Hepatology, Osaka General Medical Center, Osaka, Osaka, Japan.

Takahiro Kodama (T)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Hayato Hikita (H)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Tomohide Tatsumi (T)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Tetsuo Takehara (T)

Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Classifications MeSH