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Elevated levels of pre-treatment lactate dehydrogenase are an unfavorable predictor factor in patients with EML4-ALK rearrangement non-small cell lung cancer treated with crizotinib

Authors Liang H, Ma D, Xu Y, Zhao J, Chen M, Liu X, Zhong W, Li J, Wang M

Received 26 April 2019

Accepted for publication 23 August 2019

Published 5 September 2019 Volume 2019:11 Pages 8191—8200

DOI https://doi.org/10.2147/CMAR.S213572

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 2

Editor who approved publication: Dr Eileen O'Reilly


Hongge Liang1, Di Ma2, Yan Xu1, Jing Zhao1, Minjiang Chen1, Xiaoyan Liu1, Wei Zhong1, Junling Li2, Mengzhao Wang1

1Department of Respiratory and Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, People’s Republic of China; 2Department of Oncology, Chinese Academy of Medical Sciences Cancer Institute and Hospital, Beijing, People’s Republic of China

Correspondence: Wei Zhong
Department of Respiratory and Critical Care Medicine, Peking Union Medical College Hospital, No. 1 Shuanfuyuan Wangfujing Dongcheng District, Beijing 100730, People’s Republic of China
Tel +86 0 106 915 5039
Email zw_pumch@126.com

Mengzhao Wang
Department of Respiratory and Critical Care Medicine, Peking Union Medical College Hospital, No. 1 Shuanfuyuan Wangfujing Dongcheng District, Beijing 100730, People’s Republic of China
Tel +86 0 106 915 5154
Email mengzhaowang@sina.com

Background: Targeted therapy is an important treatment for advanced non-small cell lung cancer (NSCLC) patients with specific genetic mutations, crizotinib can prolong survival in advanced NSCLC patients with echinoderm microtubule-associated protein-like 4–anaplastic lymphoma kinase (EML4-ALK) rearrangement. We performed a retrospective analysis to investigate the association between the lactate dehydrogenase (LDH) levels and progression-free survival (PFS) in patients with EML4-ALK rearrangement NSCLC receiving treatment with crizotinib.
Methods: Advanced (stage IIIb–IV) NSCLC patients with EML4-ALK rearrangement receiving treatment with crizotinib were enrolled between January 2007 and January 2016 at Peking Union Medical College and Cancer Hospital Chinese Academy of Medical Sciences.
Results: Overall, 212 patients were enrolled. Kaplan–Meier univariate analysis showed that elevated pre-treatment LDH level (7.9 vs 14.1 months, HR =1.251, CI: 1.008–1.553, P=0.004) was significantly associated with shorter PFS, while the post-treatment mean-LDH level (13.3 vs 14.3 months, HR=1.439, 95% CI: 0.994–2.082, P=0.970) was not significantly associated with PFS. Cox proportional hazards model also identified that pre-treatment LDH level (HR=2.085, 95% CI: 1.150–3.781, P=0.016) was associated with the PFS. Logistic regression analysis showed that post-treatment LDH level was associated with creatine kinase (OR=6.712, 95% CI 3.395–13.273, P<0.01), creatine kinase isoenzyme (OR=6.297, 95% CI 2.953–13.427, P<0.01), and hemoglobin (OR=4.163, 1.741–9.956, P<0.001).
Conclusion: An elevated pre-treatment serum LDH level (>250 U/L) was significantly associated with shorter PFS in patients with EML4-ALK rearrangement NSCLC. Post-treatment elevated serum LDH level was not significantly associated with PFS, which related to adverse events including muscle damage and anemia.

Keywords: non-small cell lung cancer, lactate dehydrogenase, crizotinib, echinoderm microtubule-associated protein-like 4–anaplastic lymphoma kinase, progression-free survival

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