TY - JOUR
T1 - Clinical and laboratory factors associated with interstitial lung disease in rheumatoid arthritis
AU - Restrepo, José Félix
AU - del Rincón, Inmaculada
AU - Battafarano, Daniel F.
AU - Haas, Roy W.
AU - Doria, Merced
AU - Escalante, Agustín
N1 - Publisher Copyright:
© 2015, International League of Associations for Rheumatology (ILAR).
PY - 2015/9/26
Y1 - 2015/9/26
N2 - Objective: The objective of this study is to examine the clinical, genetic, and environmental factors associated with interstitial lung disease (ILD) in rheumatoid arthritis (RA). Method: We recruited patients with RA from rheumatology practices at the time of a scheduled visit. Each patient participated in a comprehensive assessment that included ascertainment of age, sex, joint tenderness and swelling, subcutaneous nodules, disease severity, use of methotrexate and prednisone, smoking status, rheumatoid factor (RF), antibodies against cyclic citrullinated peptide (anti-CCP),erythrocyte sedimentation rate (ESR), the 28-joint Disease Activity Score (DAS28), and the presence of the HLA–DRB1 shared epitope (SE). As part of a thorough quantification of comorbidity, we identify all comorbid conditions, including ILD. We examined variables associated with ILD using logistic regression. We tested interaction terms between SE and other covariates. Results: We studied 779 RA patients, among whom, ILD was recognized clinically in 69 (8.8 %). Variables significantly associated with ILD in a multivariable analysis included male sex, RA duration, the ESR, the DAS28, anti-CCP, and RF. There was a significant interaction between the HLA–DRB1 SE and smoking, ILD being associated with smoking only in the presence of SE. The association between ILD and anti-CCP, RF, and the ESR displayed a biological gradient, higher titers being more strongly associated with ILD. Conclusion: Anti-CCP antibodies and the RF may be pathogenically related to ILD. The association between ILD and smoking is dependent on the HLA–DRB1 SE, which may reflect gene–environment interaction.
AB - Objective: The objective of this study is to examine the clinical, genetic, and environmental factors associated with interstitial lung disease (ILD) in rheumatoid arthritis (RA). Method: We recruited patients with RA from rheumatology practices at the time of a scheduled visit. Each patient participated in a comprehensive assessment that included ascertainment of age, sex, joint tenderness and swelling, subcutaneous nodules, disease severity, use of methotrexate and prednisone, smoking status, rheumatoid factor (RF), antibodies against cyclic citrullinated peptide (anti-CCP),erythrocyte sedimentation rate (ESR), the 28-joint Disease Activity Score (DAS28), and the presence of the HLA–DRB1 shared epitope (SE). As part of a thorough quantification of comorbidity, we identify all comorbid conditions, including ILD. We examined variables associated with ILD using logistic regression. We tested interaction terms between SE and other covariates. Results: We studied 779 RA patients, among whom, ILD was recognized clinically in 69 (8.8 %). Variables significantly associated with ILD in a multivariable analysis included male sex, RA duration, the ESR, the DAS28, anti-CCP, and RF. There was a significant interaction between the HLA–DRB1 SE and smoking, ILD being associated with smoking only in the presence of SE. The association between ILD and anti-CCP, RF, and the ESR displayed a biological gradient, higher titers being more strongly associated with ILD. Conclusion: Anti-CCP antibodies and the RF may be pathogenically related to ILD. The association between ILD and smoking is dependent on the HLA–DRB1 SE, which may reflect gene–environment interaction.
KW - Anti-cyclic citrullinated antibodies
KW - Erythrocyte sedimentation
KW - HLA–DRB1
KW - Interstitial lung disease
KW - Rheumatoid arthritis
KW - Rheumatoid factor
KW - Smoking
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U2 - 10.1007/s10067-015-3025-8
DO - 10.1007/s10067-015-3025-8
M3 - Article
C2 - 26255186
AN - SCOPUS:84940437361
SN - 0770-3198
VL - 34
SP - 1529
EP - 1536
JO - Clinical Rheumatology
JF - Clinical Rheumatology
IS - 9
ER -