Anti-citrullinated protein antibody profiles predict changes in disease activity in patients with rheumatoid arthritis initiating biologics RHEUMATOLOGY Aripova, N., Kremer, J. M., Pappas, D. A., Reed, G., England, B. R., Robinson, B. H., Curtis, J. R., Thiele, G. M., Mikuls, T. R. 2023

Abstract

To determine whether an expanded antigen-specific anti-citrullinated protein antibody (ACPA) profile predicts changes in disease activity in patients with rheumatoid arthritis (RA) initiating biologics.The study included participants from a prospective, non-randomized, observational RA cohort. For this sub-study, treatment groups of interest included biologic-naïve initiating anti-TNF, biologic-exposed initiating non-TNF, and biologic-naïve initiating abatacept. ACPAs to 25 citrullinated peptides were measured using banked enrolment serum. Principal component analysis (PCA) was performed and associations of resulting principal component (PC) scores (in quartiles) and anti-CCP3 antibody (=15, 16-250 or?>?250?U/ml) with EULAR (good/moderate/none) treatment response at 6-months were examined using adjusted ordinal regression models.Participants (n?=?1092) had a mean age of 57 (±13) years and 79% were women. At 6-months, 68.5% achieved a moderate/good EULAR response. There were 3 PCs that cumulatively explained 70% of variation in ACPA values. In models including the 3 components and anti-CCP3 antibody category, only PC1 and PC2 were associated with treatment response. The highest quartile for PC1 (OR 1.76; 95% CI 1.22-2.53) and for PC2 (OR 1.74; 95% CI 1.23-2.46) were associated with treatment response after multivariable adjustment. There was no evidence of interaction between PCs and treatment group in EULAR responses (p-for-interaction >0.1).An expanded ACPA profile appears to be more strongly associated with biologic treatment response in RA than commercially available anti-CCP3 antibody levels. However, further enhancements to PCA will be needed to effectively prioritize between different biologics available for the treatment of RA.

View details for DOI 10.1093/rheumatology/kead260

View details for Web of Science ID 001011173700001

View details for PubMedID 37252826