Abstract Background Pulmonary mucinous adenocarcinoma (PMA) is a rare form of lung cancer with a low incidence rate2. It typically presents with nonspecific clinical features that mimic other infectious or inflammatory processes2. Consequently, patients often undergo multiple courses of antibiotic therapy before definitive oncologic diagnosis4. In cases suspicious for pneumonia unresponsive to treatment, early percutaneous lung biopsy, tracheoscopy, or bronchoscopy is crucial for accurate histopathologic evaluation9. However, the literature indicates that PMA’s molecular and immunophenotypic profile can overlap with other conditions and restrict treatment options7. Case Summary A 79-year-old man presents with a 3-month history of progressively worsening cough, congestion, sputum production, and dyspnea. One month earlier, bronchoscopy was negative for malignancy, and he was discharged on supplemental oxygen and corticosteroids, which did not alleviate his symptoms. Upon readmission for respiratory decompensation, a non-contrast chest CT revealed diffuse patchy opacities, concerning for organizing pneumonia. Despite broad-spectrum antibiotics and intensified steroid therapy, his respiratory status deteriorated, requiring intubation for acute hypoxic respiratory failure. Two bronchoalveolar lavage (BAL) procedures yielded negative infectious workups, including tests for bacterial, mycobacterial, fungal, viral, and atypical pathogens. Autoimmune markers (ANA, dsDNA, CCP, IL2RA, ACE) were unrevealing; WBC and CRP were elevated. Repeated chest imaging showed progressive and diffuse worsening despite therapy. Endobronchial ultrasound guided biopsy was performed and confirmed mucinous adenocarcinoma with positive CK7 and negative TTF-1, CK20, CDX2, and PD-L1. He received one dose of carboplatin/pemetrexed; however, he continued to clinically deteriorate. Conclusion Pulmonary mucinous adenocarcinoma (PMA), comprising up to 10% of lung adenocarcinomas1, is an aggressive subtype often mistaken for pneumonia, resulting in multiple courses of antibiotics and delayed oncologic intervention4. Radiologically, PMA can present as solitary nodules, ground-glass opacities, or diffuse consolidation; multifocal and multi-lobar pneumonic patterns further mimic infectious or inflammatory processes5. Hallmark features are goblet or columnar tumor cells with abundant intracytoplasmic mucin vacuoles5. Markers such as positive CK7 and negative TTF-1, CK20, and CDX2 are specific for PMA, as found in this patient8. KRAS mutations (detected in 50-76% of PMA cases) have critical implications in guiding treatment decisions1, yet both standard platinum-based chemotherapy and targeted KRAS G12C inhibitors that have emerged recently are suboptimal6. In this case, testing for KRAS mutations was not performed; however, KRAS positivity is associated with worse prognosis3. This case highlights the importance of early recognition and overviews the diagnostic/therapeutic hurdles in PMA management4. This abstract is funded by: N/A
Chukwuma et al. (Fri,) studied this question.