Brief Report: Airways abnormalities and rheumatoid arthritis–related autoantibodies in subjects without arthritis: Early injury or initiating site of autoimmunity?
Article first published online: 25 MAY 2012
Copyright © 2012 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 64, Issue 6, pages 1756–1761, June 2012
How to Cite
Demoruelle, M. K., Weisman, M. H., Simonian, P. L., Lynch, D. A., Sachs, P. B., Pedraza, I. F., Harrington, A. R., Kolfenbach, J. R., Striebich, C. C., Pham, Q. N., Strickland, C. D., Petersen, B. D., Parish, M. C., Derber, L. A., Norris, J. M., Holers, V. M. and Deane, K. D. (2012), Brief Report: Airways abnormalities and rheumatoid arthritis–related autoantibodies in subjects without arthritis: Early injury or initiating site of autoimmunity?. Arthritis & Rheumatism, 64: 1756–1761. doi: 10.1002/art.34344
- Issue published online: 25 MAY 2012
- Article first published online: 25 MAY 2012
- Accepted manuscript online: 19 DEC 2011 10:57AM EST
- Manuscript Accepted: 13 DEC 2011
- Manuscript Received: 4 MAR 2011
- NIH. Grant Numbers: AR-051461, AI-50864, AR-051394
- American College of Rheumatology Research and Education Foundation (Within Our Reach Program grant)
- Walter S. and Lucienne Driskill Foundation
To evaluate the presence of pulmonary abnormalities in rheumatoid arthritis (RA)–related autoantibody–positive subjects without inflammatory arthritis.
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.
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.
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.