Randomized trial observes NSAID-associated COP in elderly smoker, highlighting thromboembolic vigilance during treatment.
Background Cryptogenic organizing pneumonia (COP) is a rare interstitial lung disease with a mean annual incidence of approximately 1.1 cases per 100,000 persons, typically affecting adults aged 50-60. Chronic eosinophilic pneumonia (CEP) is even rarer (0.23-0.5 per 100,000), predominantly affecting middle-aged, non-smoking women. Both conditions infrequently present with acute hypoxemic respiratory failure, particularly in elderly patients with heavy smoking histories, making such presentations highly atypical and diagnostically challenging. Case Presentation An 81-year-old woman with mitral valve prolapse, hyperlipidemia, sciatica, and a 55-pack-year smoking history (quit 7/2025) presented with progressive dyspnea and intermittent wheezing following recurrent hospitalizations for multifocal pneumonia. She reported daily NSAID use (ibuprofen) for chronic sciatica. HRCT revealed upper-lobe predominant septal thickening, pleural effusions, peripheral consolidations, and mediastinal lymphadenopathy. BAL demonstrated 15% eosinophils; peripheral eosinophilia was present. Comprehensive autoimmune and infectious evaluations were negative. Transbronchial Biopsy (08/2025) of left lower lobe and lingula specimens demonstrated normal alveolar tissue and bronchial epithelium with no evidence of malignancy, excluding neoplastic etiologies. Based on temporal NSAID exposure, steroid responsiveness, and worsening dyspnea during prednisone taper from 40 to 20 mg, the working diagnosis was NSAID-associated COP, favored over CEP. The rapid relapse upon tapering is characteristic of COP, while the patient’s age, sex, and smoking history make CEP less likely. During steroid taper, she developed acute dyspnea and was diagnosed with bilateral pulmonary embolism (intermediate risk) without right heart strain. NSAIDs were discontinued; prednisone taper continued cautiously, and anticoagulation initiated for PE. At 3-month follow-up, the patient reported marked improvement in respiratory symptoms, and imaging revealed interval improvement in pulmonary consolidations and mediastinal lymphadenopathy, consistent with an inflammatory, drug-related process. Discussion and Conclusion This case highlights the rarity and diagnostic complexity of NSAID-associated COP in an elderly smoker presenting with acute hypoxemic respiratory failure. Symptom relapse during steroid taper distinguishes COP from CEP, and the temporal association with PE underscores the need for thromboembolic vigilance during glucocorticoid therapy. Transbronchial biopsy confirmed absence of malignancy, supporting a drug-induced inflammatory etiology. Literature suggests that glucocorticoids can induce a procoagulant state by increasing clotting factors, impairing fibrinolysis, and altering endothelial function, placing COP patients at risk for VTE, particularly during initiation or tapering of therapy. This case underscores the importance of medication review, careful steroid management, and awareness of thromboembolic risk in elderly patients with COP. This abstract is funded by: none
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