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Abstract Number: 1916

Antibodies to Malondialdehyde-Acetaldehyde (MAA) Modified Proteins Predict Incident Rheumatoid Arthritis-Associated Interstitial Lung Disease

Bryant England1, Geoffrey Thiele1, Dana Ascherman2, Michael Duryee1, Carlos Hunter1, Yangyuna Yang1, Punyasha Roul1, Harlan Sayles1, Andreas Reimold3, Gail Kerr4, Joshua Baker5, Jill Poole1 and Ted Mikuls1, 1University of Nebraska Medical Center, Omaha, NE, 2University of Pittsburgh, Pittsburgh, PA, 3University of Texas – Southwestern Medical Center/Dallas Veterans Affairs Medical Center (VAMC), Dallas, TX, 4Washington D.C., Veterans Affairs Medical Center (VAMC)/Georgetown and Howard Universities, Washington, DC, 5University of Pennsylvania, Philadelphia, PA

Meeting: ACR Convergence 2021

Keywords: Autoantibody(ies), interstitial lung disease, rheumatoid arthritis

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Session Information

Date: Tuesday, November 9, 2021

Session Title: Abstracts: RA – Diagnosis, Manifestations, & Outcomes II: Heart & Lung (1915–1918)

Session Type: Abstract Session

Session Time: 2:15PM-2:30PM

Background/Purpose: Because interstitial lung disease (ILD) causes substantial morbidity and mortality in rheumatoid arthritis (RA), there is a need for methods to facilitate early identification and diagnosis. Peripheral biomarkers including RA-autoantibodies, inflammatory cytokines/chemokines, and tissue remodeling proteins identify patients with established RA-ILD. Less is known, however, whether peripheral biomarkers predict incident RA-ILD. This is particularly relevant as the RA-related autoantibodies, anti-CCP and RF, are not highly predictive of future ILD risk (Natalini JG. Ann Am Thorac Soc 2021). Previously, antibodies to malondialdehyde-acetaldehyde adducts (anti-MAA), a RA-related autoantibody, were found to be closely associated with prevalent RA-ILD (England BR. Arthritis Rheumatol 2019). In this study, we aimed to determine if anti-MAA antibodies were associated with risk of incident RA-ILD.

Methods: We studied participants in the Veterans Affairs Rheumatoid Arthritis registry, a prospective cohort of U.S. Veterans with RA. Patients with RA-ILD at the time of enrollment were excluded. Demographics, smoking status, and RA measures were collected from the registry. We measured anti-MAA antibody concentrations (IgA, IgM, and IgG) by ELISA on banked serum from registry enrollment for both MAA-modified albumin and MAA-modified collagen. Anti-MAA antibody values were log-transformed, standardized, and categorized into quartiles. Incident ILD consisted of ILD diagnoses occurring after registry enrollment, determined through a previously validated approach that included systematic review of medical records for clinical diagnoses, imaging findings, and biopsy reports. In sensitivity analyses, we excluded ILD cases developing ILD within 1 year of enrollment. Multivariable Cox regression models assessed associations of anti-MAA antibody with incident ILD adjusting for age, sex, race, smoking status, anti-CCP antibody positivity, and enrollment DAS28.

Results: Among 2,317 RA patients, 190 developed ILD over 18,044 patient-years of follow-up. Patients were male predominant (90%), with a mean age of 64 years, and had frequent smoking history (79%) and anti-CCP antibody positivity (77%). Higher IgA and IgM anti-MAA-albumin antibody concentrations were associated with an increased risk of incident RA-ILD (Table 1). Effect sizes were smaller for IgG and were not statistically significant. Those with the highest quartiles of IgA and IgM anti-MAA-albumin antibodies had a higher risk of incident ILD (Q4 vs Q1 HR: IgA 1.66 [1.03, 2.67], IgM 1.74 [1.06, 2.85]; Figure 1). In contrast, anti-MAA-collagen antibodies were not significantly associated with incident RA-ILD risk (Table 1). Results were consistent in sensitivity analysis excluding ILD cases occurring in the first year after registry enrollment (Table 1).

Conclusion: Serum anti-MAA-albumin antibodies are associated with a higher risk of developing ILD among RA patients. These findings highlight the role novel autoantibodies may serve in the pathogenesis of RA-ILD as well as support the development of risk models to predict ILD onset.

Table 1. Associations of anti-MAA antibodies with incident RA-ILD.

Figure 1. RA-ILD free survival by quartiles of anti-MAA-albumin antibodies. Values hazards ratios (95% confidence intervals) from Cox regression models adjusted for age, sex, race, smoking status, anti-CCP antibody positivity, and DAS28.


Disclosures: B. England, Boehringer-Ingelheim, 2; G. Thiele, Regeneron, 6; D. Ascherman, None; M. Duryee, None; C. Hunter, None; Y. Yang, None; P. Roul, None; H. Sayles, None; A. Reimold, None; G. Kerr, Aurinia, 6, Novartis, 5, Bristol Myers Squibb, 1, 5, Pfizer, 1, Horizon, 1; J. Baker, Bristol-Myers Squib, 2, Pfizer, 2; J. Poole, None; T. Mikuls, Gilead Sciences, 2, Horizon, 2, 5, Pfizer Inc, 2, Sanofi, 2, Bristol-Myers Squibb, 2.

To cite this abstract in AMA style:

England B, Thiele G, Ascherman D, Duryee M, Hunter C, Yang Y, Roul P, Sayles H, Reimold A, Kerr G, Baker J, Poole J, Mikuls T. Antibodies to Malondialdehyde-Acetaldehyde (MAA) Modified Proteins Predict Incident Rheumatoid Arthritis-Associated Interstitial Lung Disease [abstract]. Arthritis Rheumatol. 2021; 73 (suppl 9). https://acrabstracts.org/abstract/antibodies-to-malondialdehyde-acetaldehyde-maa-modified-proteins-predict-incident-rheumatoid-arthritis-associated-interstitial-lung-disease/. Accessed January 30, 2023.
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