B80-5-46 A Masked Presentation of Predominant Lepidic Growth Lung Adenocarcinoma

Abstract Once Non-mucinous Bronchoalveolar Carcinoma (BAC), now Lepidic Predominant Adenocarcinoma (LPA) is defined by bronchioalveolar pattern characterized by growth along alveolar septae without extension into nearby tissues1. Lepidic spread may be involved in up to 19.3% of lung adenocarcinomas2, and has excellent prognosis after surgical resection3,4. This patient’s presentation however was masked beneath a complex pulmonary history, masquerading as non-resolving ground glass opacities that led to delays in diagnosis. 48 year-old woman with asthma, recurrent pneumonias, Interstitial Lung Disease (ILD) with 2L home O2, and 6-pack-year smoking history quit 18 years prior, presented with hypoxia. Chest Xray showed nonspecific interstitial changes, and CT angiogram demonstrated subpleural infiltrates in right lung lobes and left lower lung, with peripheral reticular opacities in bilateral upper lobes without nodules. Bronchoscopy with transbronchial biopsy was performed for suspicion of worsening ILD, showed chronic inflammation without infection or malignancy. The patient was treated for severe persistent asthma and viral pneumonia over the next several months, with symptoms improving on prednisone. CT chest later showed nonspecific reticular opacities and similar subpleural cystic changes, and the patient was referred for lung transplant. Their respiratory status deteriorated and she underwent Video-Assisted-Thoracic-Surgery (VATS) with wedge biopsy of multiple lobes; pathology returned as LPA. Subsequent PET scan revealed left lung involvement as well. She was staged T4N0M1a. She trialed various treatments over the next year, but her disease demonstrated resistance to carboplatin, pemetrexed, pembrolizumab, dabrafenib, trametinib, docetaxel, and ramucirumab, with progression in bilateral lungs, mediastinal and axillary lymph nodes. The patient eventually passed while hospitalized for malignant pleural effusions. On CT, LPA typically presents a ground-glass dominant opacities; late in progression, there may be nodularities that indicate invasion1,3,4. Here, LPA emerged as nonspecific ground-glass opacities without alarm features.- The indolent radiographic appearance and symptomatic responsiveness to steroids can mimic infectious or fibrotic lung disease, delaying appropriate oncological workup. In patients with autoimmune or interstitial lung disease, particularly persistent or multifocal ground-glass opacities unresponsive to standard therapies, biopsy with histopathological evaluation is warranted.- Improvement with steroids does not exclude malignancy. Symptomatic relief may reflect improvement in tumor inflammation.6 This case illustrates the diagnostic challenges of LPA concealed by complex pulmonary history. A high index of suspicion is critical with non-resolving opacities, even in younger or non-smoking individuals. LPA can pose as benign or autoimmune pulmonary processes. Diagnosis relies on recognition of uncommon variants of lung malignancy before they outgrow their indolent phases. This abstract is funded by: None