Leukoencephalopathy caused by epidermal growth factor tyrosine kinase inhibitor: A case report

초록

Introduction Leukoencephalopathy is a pathological appearance of the brain white matter seen as periventricular hyperintensities on T2 MR imaging. Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) are associated with mild neurological symptoms but relatively unknown for serious central neuropathy, especially leukoencephalopathy. Here, we report the first case of leukoencephalopathy caused by EGFR TKI. Case Report A 57-year-old woman was referred because of catatonia. Chest CT showed right upper lobe mass. Histological examination showed an adenocarcinoma with EGFR19 deletion. Multiple parenchymal and diffuse leptomeningeal metastasis were suspected on brain MRI. Erlotinib is administered. She had achieved a partial response and her symptom improved. After 2 years of treatment, she complained of dysarthria. Brain MRI revealed leukoencephalopathy without metastasis. Despite discontinuation of treatment, her symptom worsened. So, retreatment was applied. Although lung cancer was not progressed for another 2 years, leukoencephalopathy was progressed. Even after permanent discontinuation of treatment, her symptom persisted and she died because of infection. Discussion Leukoencephalopathy is subclinical and mostly transient but some rare patients have extensive signal change and rapid irreversible neurological deterioration. Although the etiology is not certain, blood-brain barrier(BBB) breakdown and endothelial dysfunction may be associated. Leukoencephalopathy is usually caused by chemo-therapy or radiotherapy but rare by EGFR TKI due to low permeability of BBB. This is the only case of leukoencephalopathy due to 1st generation TKI. However, as the 3rd generation TKIs that penetrate BBB are widely used, it should be suspect neurological toxicity such as leukoencephalopathy when neurological symptoms appear. Conflict of Interest No potential conflict of interest relevant to this article was reported.