A72-13 Fibrotic Lung Disease in Cystic Fibrosis: The Overlooked Role of Vaping and COVID-19

Abstract Introduction Cystic fibrosis (CF) is a multisystem genetic disorder characterized by chronic respiratory infections, airway inflammation, and progressive structural lung damage, including bronchiectasis. While bronchiectasis is a well-recognized complication, the development of fibrotic lung disease is less defined and may be influenced by environmental and infectious factors. Emerging evidence suggests that inhalational exposures such as e-cigarette use and viral infections like SARS-CoV-2 may accelerate lung injury and fibrosis, particularly in individuals with pre-existing disease. This case highlights the potential contribution of these factors to fibrotic lung changes in CF. Case Description A 52-year-old male with cystic fibrosis complicated by bronchiectasis and pancreatic involvement presented with worsening oxygen requirements, cough, and thickened mucus. His history included daily e-cigarette use and a recent SARS-CoV-2 infection. Oxygen saturation was 85% at rest on his baseline 2 L nasal cannula. Exam revealed diffuse bilateral crackles. Chest CT showed diffuse bronchial wall thickening, bronchiectasis, bronchiolectasis, and regional volume loss with reticulation, architectural distortion, and traction bronchiectasis consistent with fibrotic lung disease. He was hospitalized and treated with broad-spectrum antibiotics and corticosteroids, leading to symptomatic improvement. Interval CTs over two years demonstrated stable fibrotic changes. Discussion Fibrotic lung disease in adults with CF represents an emerging clinical challenge as survival improves. The mechanisms are incompletely understood but likely involve chronic inflammation, infection, and repeated structural injury that trigger aberrant repair and remodeling. E-cigarette use may add further insult. Vaping has been linked to airway inflammation, epithelial injury, oxidative stress, and progressive fibrosis. Though most reports emphasize acute lung injury, chronic exposure may drive subclinical and cumulative damage, particularly in those with underlying airway disease. Similarly, SARS-CoV-2 infection has been associated with persistent interstitial abnormalities and post-infectious fibrosis. In CF, viral injury layered upon pre-existing bronchiectasis and inflammation may accelerate irreversible architectural distortion and lung function decline. This case illustrates how overlapping factors—CF pathology, vaping, and COVID-19—can synergistically promote fibrotic remodeling. The chronic stability of these changes underscores the potential for lasting structural damage even after clinical recovery. Clinicians should counsel CF patients on avoiding modifiable exposures such as vaping, maintain vigilant post-viral follow-up, and consider early referral for pulmonary rehabilitation or transplant evaluation when fibrosis emerges. Increased awareness of this multifactorial pathway is critical to preventing further decline. This abstract is funded by: None