Brief Report: Airways abnormalities and rheumatoid arthritis-related autoantibodies in subjects without arthritis: Early injury or initiating site of autoimmunity?

Objective To evaluate the presence of pulmonary abnormalities in rheumatoid arthritis (RA)–related autoantibody–positive subjects without inflammatory arthritis. Methods Forty‐two subjects who did not have inflammatory arthritis but were positive for anti–cyclic citrullinated peptide antibodies and/...

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Published inArthritis & rheumatology (Hoboken, N.J.) Vol. 64; no. 6; pp. 1756 - 1761
Main Authors Demoruelle, M. Kristen, Weisman, Michael H., Simonian, Philip L., Lynch, David A., Sachs, Peter B., Pedraza, Isabel F., Harrington, Annie R., Kolfenbach, Jason R., Striebich, Christopher C., Pham, Quyen N., Strickland, Colin D., Petersen, Brian D., Parish, Mark C., Derber, Lezlie A., Norris, Jill M., Holers, V. Michael, Deane, Kevin D.
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.06.2012
Wiley Subscription Services, Inc
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Summary:Objective To evaluate the presence of pulmonary abnormalities in rheumatoid arthritis (RA)–related autoantibody–positive subjects without inflammatory arthritis. Methods Forty‐two subjects who did not have inflammatory arthritis but were positive for anti–cyclic citrullinated peptide antibodies and/or ≥2 rheumatoid factor isotypes (a profile that is 96% specific for RA), 15 autoantibody‐negative controls, and 12 patients with established seropositive early RA (<1‐year duration) underwent spirometry and high‐resolution computed tomography (HRCT) lung imaging. Results The median age of autoantibody‐positive subjects was 54 years, 52% were female, and 38% were ever‐smokers; these characteristics were not significantly different from those of autoantibody‐negative control subjects. No autoantibody‐positive subject had inflammatory arthritis based on joint examination. HRCT revealed that 76% of autoantibody‐positive subjects had airways abnormalities including bronchial wall thickening, bronchiectasis, centrilobular opacities, and air trapping, compared with 33% of autoantibody‐negative controls (P = 0.005). The prevalence and type of lung abnormalities among autoantibody‐positive subjects were similar to those among patients with early RA. In 2 autoantibody‐positive subjects with airways disease, inflammatory arthritis classifiable as articular RA developed ∼13 months after the lung evaluation. Conclusion Airways abnormalities that are consistent with inflammation are common in autoantibody‐positive subjects without inflammatory arthritis and are similar to airways abnormalities seen in patients with early RA. These findings suggest that the lung may be an early site of autoimmune‐related injury and potentially a site of generation of RA‐related autoimmunity. Further studies are needed to define the mechanistic role of lung inflammation in the development of RA.
Bibliography:Walter S. and Lucienne Driskill Foundation
ark:/67375/WNG-3V3DTGM8-4
ArticleID:ART34344
NIH - No. AR-051461; No. AI-50864; No. AR-051394
American College of Rheumatology Research and Education Foundation (Within Our Reach Program grant)
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ISSN:0004-3591
2326-5191
1529-0131
2326-5205
DOI:10.1002/art.34344