Session Type: ACR Poster Session C
Session Time: 9:00AM-11:00AM
Background/Purpose: Interstitial lung disease (ILD) is an extra-articular manifestation of rheumatoid arthritis (RA) which contributes to increased morbidity and mortality. Clinico-epidemiological data indicate some overlap in disease course between RA-ILD and idiopathic pulmonary fibrosis (IPF), particularly in subsets of RA-ILD patients with UIP-like pathology. We therefore evaluated levels of specific peripheral blood protein markers in patients with RA-ILD and IPF to determine molecular profiles indicative of shared disease pathogenesis.
Methods: A cohort of patients that met ACR classification criteria for rheumatoid arthritis were enrolled and subclassified as having RA-no ILD versus RA-ILD (mild vs. advanced parenchymal lung abnormalities) based on high resolution computed tomography scans of the chest (HRCT). A cohort of patients with IPF was also enrolled through Brigham and Women’s Hospital. Standard solid phase enzyme-linked immunosorbent assays (ELISAs) were used to assess serum levels of matrix metalloproteinase 7 (MMP-7) and interferon-ϒ-inducible protein 10 (IP-10), which had previously been found to be significantly elevated in RA-ILD. Levels of serum biomarkers were compared using Mann U Whitney testing.
Results: 71 patients with RA were enrolled and classified as RA-no ILD (n=22) versus RA-ILD (n=49). Serum specimens were obtained from these patients as well as a comparator cohort of IPF patients (n=44). 72.7% (n=16) of patients in the RA-no ILD group, 63.3% (n=31) of patients in the RA-ILD and 40.9% (n=18) of patients in the IPF group were women. The average age of the patients in the RA-ILD and IPF groups were 65 and 66 years, respectively, vs 50 years in the RA-no ILD group (p=<0.0001).
Conclusion: Serum levels of both MMP-7 and IP-10 were elevated in patients with IPF and RA-ILD relative to RA patients without evidence of ILD. This overlap in biomarker signatures encompassing both inflammatory (IP-10) and remodeling (MMP-7) pathways supports a possible link in pathogenesis that may suggest common therapeutic targets in RA-ILD and IPF.
To cite this abstract in AMA style:Fernandez K, Doyle T, Harlow L, Rosas IO, Ascherman DP. Common Biomarker Elevations in Idiopathic Pulmonary Fibrosis and Rheumatoid Arthritis-Associated Interstitial Lung Disease [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/common-biomarker-elevations-in-idiopathic-pulmonary-fibrosis-and-rheumatoid-arthritis-associated-interstitial-lung-disease/. Accessed October 30, 2020.
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