Rheumatoid arthritis (RA)-specific autoantibodies in patients with interstitial lung disease and absence of clinically apparent articular RA.

Rheumatoid arthritis (RA)-specific autoantibodies in patients with interstitial lung disease and absence of clinically apparent articular RA.
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DOI:
10.1007/s10067-009-1128-9
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发表时间:
2009-05
影响因子:
3.4
通讯作者:
Deane, Kevin D.
Deane, Kevin D.
中科院分区:
医学3区
文献类型:
--
作者:
Gizinski, Alison M.;Mascolo, Margherita;Loucks, Jennifer L.;Kervitsky, Alma;Meehan, Richard T.;Brown, Kevin K.;Holers, V. Michael;Deane, Kevin D.

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本研究的目的是在间质性肺病(ILD)受试者中识别类风湿关节炎(RA)相关自身抗体,无RA关节表现,支持RA相关自身免疫可能在非关节部位(如肺)产生的假设。这是一项回顾性图表审查,利用ILD患者的临床数据库识别肺部疾病、RA相关自身抗体阳性且无关节RA临床证据的病例。4例ILD、RF和抗CCP阳性且无RA关节发现的患者被确定。所有4例患者均为男性,诊断ILD时的平均年龄为70岁。他们都有吸烟史。3例患者在ILD诊断后2年内死亡,从未出现与RA一致的关节症状;最后一例患者在停止ILD免疫抑制治疗后数月符合关节RA的全部标准。RF和抗CCP可存在于患有ILD但无关节性RA临床证据的吸烟者中,在1例病例中,症状性ILD和自身抗体阳性先于关节性RA的发展。这些发现表明,RA特异性自身免疫可能是由于肺内的免疫相互作用而产生的,并可能与吸烟等环境因素有关。
The purpose of this study was to identify rheumatoid arthritis (RA)-related autoantibodies in subjects with interstitial lung disease (ILD) and no articular findings of RA, supporting the hypothesis that RA-related autoimmunity may be generated in non-articular sites, such as the lung. This was a retrospective chart review utilizing clinic databases of patients with ILD to identify cases with lung disease, RA-related autoantibody positivity, and no clinical evidence of articular RA. Four patients with ILD, RF, and anti-CCP positivity and no articular findings of RA were identified. All four patients were male with a mean age at time of diagnosis of ILD of 70 years old. All had a history of smoking. Three patients died within 2 years of diagnosis of ILD and never developed articular symptoms consistent with RA; the final case met full criteria for articular RA several months after stopping immunosuppressive treatment for ILD. RF and anti-CCP can be present in smokers with ILD without clinical evidence of articular RA and in one case symptomatic ILD and autoantibody positivity preceded the development of articular RA. These findings suggest that RA-specific autoimmunity may be generated due to immunologic interactions in the lung and may be related to environmental factors such as smoking.
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