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The following is a summary of “Peripheral Biomarker Signatures in Rheumatoid Arthritis-Associated Interstitial Lung Disease,” published in the March 2025 issue of Arthritis & Rheumatology by Wheeler et al. 

Rheumatoid arthritis (RA)-associated interstitial lung disease (RA-ILD) causes high morbidity and mortality in RA. Effective risk stratification remains a challenge. 

Researchers conducted a retrospective study to identify peripheral blood biomarker signatures in RA that enhance RA-ILD discrimination beyond clinical and genetic risk factors. 

They conducted a cross-sectional study using the Veterans Affairs Rheumatoid Arthritis (VARA) registry. ILD was validated through record review. They measured 14 autoantibodies, 36 cytokines/chemokines, 3 adipokines, 3 alarmins, and 9 matrix metalloproteinases from serum or plasma. MUC5B rs35705950 genotyping was obtained via microarray. They used principal component analysis (PCA) for biomarker signatures and logistic regression to compare models predicting RA-ILD. 

The results showed that among 2,001 participants with RA (88.7% male, mean age 63.7 years), 121 (6.4%) had RA-ILD. About 15 PCs were identified, with eight linked to RA-ILD after adjusting for clinical factors. These included innate and allergic responses, autoantibodies (anti-CCP, RF, anti-MAA), adipokines, alarmins, tissue remodeling, and neutrophil chemotaxis. Models with PCs (area under the curve [AUC] 0.739) and PCs + MUC5B (AUC 0.751) outperformed clinical risk factors alone (AUC 0.630; P<0.001). 

Investigators found that peripheral biomarker signatures were associated with RA-ILD and improved its identification beyond clinical risk factors. These findings suggested diverse pathways were involved in RA-ILD pathogenesis. 

Source: acrjournals.onlinelibrary.wiley.com/doi/abs/10.1002/art.43149