4.5 Article

Alectinib for Miliary Lung Metastasis in ALK-Positive Lung Adenocarcinoma

Journal

ONCOTARGETS AND THERAPY
Volume 14, Issue -, Pages 2911-2915

Publisher

DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S300229

Keywords

alectinib; ALK rearrangement; non-small-cell lung cancer; miliary pulmonary metastasis

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This case report described a 32-year-old female patient with ALK-rearranged non-small cell lung cancer presenting with miliary pulmonary metastasis and elevated serum amylase level. Treatment with alectinib resulted in regression of CT findings and decrease in serum amylase level. It emphasizes the importance of comprehensive driver mutation testing in young patients with miliary pulmonary metastasis.
Background: Miliary pulmonary metastasis characterized by tiny nodules is a rare metastatic pattern in advanced non-small cell lung cancer (NSCLC) and is usually seen in patients harboring an EGFR mutation, and amylase-producing lung cancer is highly uncommon and rarely reported in NSCLC patients who have an EGFR mutation. Case: A 32-year-old Japanese female was found to have miliary pulmonary nodules throughout both lung fields on a chest x-ray examination during an annual health checkup. Further examination by computed tomography (CT) revealed diffuse, bilateral, miliary nodules. Blood tests showed no increased tumor marker levels, but there was a significantly increased serum amylase level. A diagnosis of ALK-rearranged adenocarcinoma was made based on the results of a mediastinal lymph node biopsy obtained by endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). Treatment with alectinib resulted in rapid regression of the CT shadows and a reduction in the patient's serum amylase level. Conclusion: We have reported a case of ALK-rearranged NSCLC with a miliary pulmonary metastasis pattern that was sensitive to alectinib and in which the serum amylase level decreased in response to treatment with alectinib. Young patients with miliary pulmonary metastasis should be checked for all driver mutations.

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