C80-53 Radiologic Suspicion of Lepidic Adenocarcinoma Despite Negative Cytology

Abstract Introduction Lepidic-predominant adenocarcinoma (LPA) is non-small cell lung cancer characterized by neoplastic cells proliferating along intact alveolar structures without stromal, vascular, or pleural invasion1. Lepidic tumors typically grow along alveolar septae without invasion2. Diagnosis can be elusive, particularly because of indolent nature and mimicry of inflammatory or infectious processes on imaging3. Case Presentation A 79-year-old male with history of CAD (s/p CABG and drug eluting stents), COPD, AFib, HTN, HLD, and kidney transplantation on immunosuppressive therapy was referred for persistent right lower lobe (RLL) consolidation after presenting in 2016 with an intermittent dry, nonproductive cough without fever, chills, upper respiratory symptoms, weight loss, or exposure to sick contacts. Previous similar episodes had resolved with corticosteroid therapy. Pulmonary symptoms recurred in 2023 without signs of infection. A bronchoscopy with bronchoalveolar lavage (BAL) revealed clear secretions most prominent in the RLL with noted collapsible medial basilar subsegment and no evidence of malignancy from cytology. A non-contrast chest CT demonstrated a dense area of consolidation in the posterior basal segment of RLL with adjacent, patchy ground-glass opacities showing a hazy increase in lung attenuation without obscuration of underlying bronchial or vascular structures. The radiographic pattern raised suspicion for neoplastic etiologies, though inflammatory or infectious causes could not be excluded. Concern for malignancy prompted CT-guided percutaneous lung biopsy, confirming LPA. Endobronchial ultrasound (EBUS) with transbronchial sampling and cytologic analysis was negative for malignancy. The patient remained clinically stable with preserved functional status and no respiratory compromise. Discussion Despite non-diagnostic pathology, persistent radiographic findings in a high-risk, immunosuppressed patient raised concern for a slow-growing malignancy such as lepidic adenocarcinoma. Serial imaging and consideration of tissue biopsy were recommended to further characterize the lesion. Our case of LPA was confirmed through pathology given the persistence of radiographic findings and a high-risk immunosuppressed patient. A previous case resort described an immunocompetent patient presenting with bilateral erosion and spread of lipidic adenocarcinoma, mimicking diffuse infectious pneumonitis, ultimately rapid clinical decline despite absence of lymphovascular or distant metastatic disease. Our case evolved from a focal consolidation in a more indolent manner, then became more invasive with diffuse ground glass and bilateral lung involvement. These cases illustrate the heterogenous clinical behavior of lipidic adenocarcinoma. In the immunocompromise state, radiographic findings can be broader and disease advancement rapid. This case shed light on the urgency of biopsy to bridge the gap between the clinical, radiologic and pathologic discordance in immunocompromise individuals. This abstract is funded by: None