Abstract Introduction Interstitial lung disease (ILD) refers to a group of disorders marked by inflammation and fibrosis of the pulmonary interstitium. Usual interstitial pneumonia (UIP) pattern is characterized on high-resolution computed tomography (HRCT) by subpleural, basal predominant reticulation, traction bronchiectasis and honeycombing.1 Rheumatoid arthritis (RA) is a systemic autoimmune disease with well-recognized extra-articular involvement.2 In RA-ILD, the UIP pattern emerges as the predominant imaging and histopathologic finding, accounting for roughly 24% of cases.3 When evaluating ILD with findings of exuberant honeycombing on HRCT, it is imperative to screen for underlying autoimmune etiologies to ensure early diagnosis and treatment. Case We present a case of a 69-year-old male with fibrotic ILD, diagnosed during previous hospitalization with CT chest findings consistent with a UIP pattern who presented for increasing shortness of breath at rest and acute on chronic hypoxemic respiratory failure. He required rapid escalation of oxygen requirements, transitioning from 5L via nasal cannula to 50L/40% high-flow nasal canula. CTA chest revealed extensive, left lower lung predominant interstitial fibrosis with honeycombing and mild traction bronchiectasis, unchanged from initial CT 10 months prior. Inflammatory and auto-immune markers were ordered, returning significant for elevated rheumatoid factor 266 and anti-cyclic citrullinated peptide 250. During hospitalization patient required temporary upgrade to ICU for acute hypercapnic respiratory failure which resolved with bilevel positive airway pressure ventilation. Given his decompensation, he was started on high-dose intravenous corticosteroids with rapid improvement in oxygenation requirements. He was subsequently placed on a prednisone taper and discharged to home, with outpatient follow-up scheduled with the ILD clinic actively pending. Discussion Patient was initially diagnosed with ILD with UIP a year ago without an identified underlying mechanism noted. The initial CT chest findings of exuberant honeycombing prompted more extensive workup including a comprehensive autoimmune panel. Resulting labs correlated clinically with the patient’s improvement with steroids. The pleural thickening noted assisted in narrowing the differential diagnosis, as it is a characteristic finding of RA.4 UIP itself is not a diagnosis and thus when observed on imaging requires further investigation towards identifying potential inciting factors, in this case rheumatoid arthritis. Conclusion This case highlights the importance of considering autoimmune etiologies, particularly rheumatoid arthritis, in patients presenting with ILD demonstrating a UIP pattern and exuberant honeycombing on imaging. Early identification of an underlying inflammatory cause allows for timely initiation of targeted immunosuppressive or antifibrotic therapy, potentially improving outcomes and slowing disease progression. This abstract is funded by: None
Stere et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: