Efficacy of epidermal growth factor receptor-tyrosine kinase inhibitors for patient with leptomeningeal metastasis of epidermal growth factor receptor mutant non-small cell lung cancer.
10.12701/yujm.2016.33.1.64
- Author:
Jong Sik LEE
1
;
Kyung Ann LEE
;
Kang Hoon LEE
;
Sun Young MOON
;
In Ae KIM
;
Sung Jin JEON
;
Jae Ki MIN
;
Hee Joung KIM
;
Kye Young LEE
Author Information
1. Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea. kyleemd@kuh.ac.kr
- Publication Type:Case Report
- Keywords:
Epidermal growth factor receptor;
Cerebrospinal fluid;
Gefitinib;
Erlotinib
- MeSH:
Adenocarcinoma;
Carboplatin;
Carcinoma, Non-Small-Cell Lung;
Central Nervous System;
Cerebrospinal Fluid;
Cisplatin;
Drug Therapy;
Epidermal Growth Factor*;
Erlotinib Hydrochloride;
Headache;
Humans;
Lung Neoplasms*;
Lung*;
Methotrexate;
Middle Aged;
Nausea;
Neoplasm Metastasis*;
Paclitaxel;
Phosphotransferases*;
Protein-Tyrosine Kinases;
Receptor, Epidermal Growth Factor*;
Recurrence;
Thorax;
Vomiting
- From:Yeungnam University Journal of Medicine
2016;33(1):64-67
- CountryRepublic of Korea
- Language:English
-
Abstract:
We report on a 64-year-old man with leptomeningeal metastasis (LM) from an epidermal growth factor receptor (EGFR)-mutated adenocarcinoma of the lung. He was treated with paclitaxel, cisplatin. After completion of chemotherapy, he complained of headache, nausea, and vomiting. EGFR-mutated tumor cells were identified from the cerebrospinal fluid (CSF). Second-line therapy with gefitinib, methotrexate was started. After receiving gefitinib for 4 weeks, he had no more headaches or vomiting. Eleven months after initiation of gefitinib, he developed headache and nausea. Chest computed tomography showed aggravation of bone metastasis. Third-line therapy was started with gemcitabine and carboplatin. Two weeks later, he experienced disorientation. After a fourth relapse within the central nervous system, the therapy was switched to erlotinib and significant improvement of LM was achieved. This case shows that LM can be diagnosed by detecting EGFR mutation in CSF and EGFR tyrosine kinase inhibitors are effective for LM from EGFR mutant non-small cell lung cancer.
