Background/Purpose:

Airways abnormalities that are consistent with inflammation are common in anti-CCP2 positive subjects without inflammatory arthritis. Anti-CCP2 antibodies are associated with HRCT parenchymal lung abnormalities in patients with early RA. This study aims to examine the association between ACPA fine specificities and HRCT lung changes in an early RA cohort and to asses these changes after 6 months.

Methods:

Patients (n=106) with newly diagnosed RA according to the ACR 1987 criteria and naïve to treatment with oral glucocorticoids or DMARDs were included. HRCT was performed in order to assess the presence parenchymal (nodules, ground-glass opacities, opacities, fibrosis, emphysema) and airway abnormalities (bronchiectasis, air trapping, air wall thickening). EliA system (Phadia) was used to detect RF IgA and IgM, anti-CCP2 IgA and IgG, and peptide microarray (Phadia) was used to detect antibodies against 10 citrullinated (Cit) peptidic antigens: CCP-1 (Filaggrin), CEP-1 (α-enolase), Vim 2-17, Vim 60-75 (Vimentin), Fib α 36-50, Fib α 573, Fib α 591, Fib α 621-635, Fib β 36-52, Fib β 60-74 (Fibrinogen). Most of the patients (n=93) were followed up after 6 months. Logistic regression analysis was performed to examine associations between HRCT lung changes at the time of RA diagnosis and autoantibodies.

Results:

HRCT parenchymal and airway changes was present in 58 (54.7%) and 68 (64.2%) patients, respectively. The forced vital capacity (FVC) was significantly lower in the presence of airway abnormalities, while the ratio FEV₁/FVC was significantly lower in patients with parenchymal lung changes. Higher age, RF IgA, CCP2 IgG, ever smoking and pack-years above 24 were significant predictors of parenchymal lung changes. Some ACPA fine specificities, especially against Cit Fib and Vim peptides, were associated to parenchymal lung changes in ever smokers. The risk of having parenchymal changes increased parallel to the increase in number of ACPA specificities. Having more than 5 ACPA specificities at the time of diagnosis increased the risk of having parenchymal lung abnormalities in current smokers (OR=13.8, 95% CI=1.0-196.2, p=0.05). Of the patients that were followed up after 6 months 4 had progression of fibrosis and 3 had new fibrosis. No difference in airway changes were observed at follow-up. There was a significant decrease in DAS28 at follow-up (Mean±SD: 5.5 ± 1.1 vs 3.2±1.3 P value < 0.001). The titers of some but not all of the ACPA fine specificity was significantly decreased after 6 months of treatment CCP-1 (Mean±SD 46.6±289.7 vs 101.6±235.3), CEP-1 (59.1±120.1 vs 35.9±76.3), Vim 60-75 (338±488.1 vs 220.3±327.2), Vim 2-17 (25.7±59.3 vs 17±37.8), Fib β 60-74 (237.3±411 vs 136.4±241.5), Fib α 621-635 (187.3±306.3 vs 115.9±203.2).

Conclusion:

The presence of RF IgA, anti-CCP2 IgG and antibodies to Cit Fib and Vim peptides were associated with parenchymal lung changes in early-untreated RA. The more ACPA fine specificities, the higher the risk of having parenchymal lung changes already at the time of RA diagnosis. Treatment with DMARDs significantly reduces the disease activity and titers of some of the ACPA fine specificities.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/number-and-type-of-acpa-fine-specificities-are-correlated-to-high-resolution-computed-tomography-parenchymal-lungs-changes-in-patients-with-early-untreated-rheumatoid-arthritis/