Brief report: airways abnormalities and rheumatoid arthritis-related autoantibodies in subjects without arthritis: early injury or initiating site of autoimmunity?
Brief report: airways abnormalities and rheumatoid arthritis-related autoantibodies in subjects without arthritis: early injury or initiating site of autoimmunity?
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简要报告:无关节炎受试者的气道异常和类风湿性关节炎相关自身抗体:早期损伤或自身免疫的起始部位?
DOI:
10.1002/art.34344
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发表时间:
2012-06
影响因子:
--
通讯作者:
Deane, Kevin D.
中科院分区:
文献类型:
--
作者:
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.
To evaluate the presence of pulmonary abnormalities in subjects with rheumatoid arthritis (RA)-related autoantibody (Ab) positivity without inflammatory arthritis (IA). 42 subjects without IA but with elevations of anti-cyclic citrullinated peptide antibodies and/or 2 or more rheumatoid factor isotypes (a profile that is 96% specific for RA), 15 Ab(−) controls and 12 patients with early established seropositive RA (<1 year duration) underwent spirometry and high-resolution computed tomographic (HRCT) lung imaging. The median age of Ab(+) subjects was 54 years-old, 52% were female and 38% were smokers (not significantly different than Ab(−) controls). No Ab(+) subject had IA on joint examination. On HRCT, 76% of Ab(+) subjects had airways abnormalities including bronchial wall thickening, bronchiectasis, centrilobular opacities and air trapping, compared to 33% of Ab(−) controls (p=0.005). The Ab(+) subjects had similar prevalence and type of lung abnormalities compared to patients with early RA. Two Ab(+) subjects with airways disease developed IA classifiable as articular RA ~13 months after lung evaluation. Airways abnormalities that are consistent with inflammation are common in Ab(+) subjects without IA, and similar to airways abnormalities seen in 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.
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