Nintedanib allows retreatment with atezolizumab of combined non-small cell lung cancer/idiopathic pulmonary fibrosis after atezolizumab-induced pneumonitis: a case report

被引:24
作者
Yamakawa, Hideaki [1 ,2 ]
Oba, Tomohiro [1 ]
Ohta, Hiroki [1 ]
Tsukahara, Yuta [1 ]
Kida, Gen [1 ]
Tsumiyama, Emiri [1 ,2 ]
Nishizawa, Tomotaka [1 ]
Kawabe, Rie [1 ]
Sato, Shintaro [1 ]
Akasaka, Keiichi [1 ]
Amano, Masako [1 ]
Kuwano, Kazuyoshi [2 ]
Matsushima, Hidekazu [1 ]
机构
[1] Saitama Red Cross Hosp, Dept Resp Med, Chuo Ku, 1-5 Shintoshin, Saitama, Saitama 3308553, Japan
[2] Tokyo Jikei Univ Hosp, Dept Resp Med, Tokyo, Japan
关键词
Nintedanib; Immune checkpoint inhibitors; Drug-induced pneumonitis; INHIBITOR-RELATED PNEUMONITIS; ADVANCED CANCER; EFFICACY; BLOCKADE; SAFETY;
D O I
10.1186/s12890-019-0920-9
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background Nintedanib is a tyrosine kinase inhibitor that efficiently slows the progression of idiopathic pulmonary fibrosis (IPF) and has an acceptable tolerability profile. In contrast, immune checkpoint inhibitors (ICIs) such as programmed death 1 and programmed death ligand 1 inhibitors have shown clinical activity and marked efficacy in the treatment of non-small cell lung cancer. However, it is unclear whether nintedanib reduces the risk of ICI-induced pneumonitis in IPF. Case presentation A 78-year-old man with squamous cell lung carcinoma in IPF underwent second-line treatment with pembrolizumab. He was diagnosed as having pembrolizumab-induced pneumonitis after two cycles. He was administered prednisolone (PSL) and then improved immediately. Thereafter, his lung cancer lesion enlarged despite treatment with TS-1. Atezolizumab was then administered as 4th-line chemotherapy, but he immediately developed atezolizumab-induced pneumonitis after 1 cycle. The re-escalated dosage of PSL improved the pneumonitis, and then nintedanib was started as additional therapy. Under careful observation with nintedanib, atezolizumab was re-administered on day 1 of an every-21-day cycle. After three cycles, it remained stable without exacerbation of drug-induced pneumonitis. Conclusion This case indicates the possibility that the addition of nintedanib to ICI therapy might prevent drug-induced pneumonitis or acute exacerbation of IPF. However, whether anti-fibrotic agents such as nintedanib are actually effective in preventing ICI-induced pneumonitis in ILD remains unknown and additional research is greatly needed to identify effective therapies for ILD combined with lung cancer.
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