Triple positivity for autoantibodies in patients with rheumatoid arthritis is associated with a severe course of the disease but not with bone turnover markers.

INTRODUCTION

Rheumatoid arthritis (RA) is a prevalent autoimmune disorder characterized by chronic joint inflammation and progressive bone erosion. Traditional autoantibodies, such as anti-citrullinated peptide antibodies (ACPAs) and rheumatoid factor (RF), are established markers associated with disease severity. Recent studies have identified anti-carbamylated protein (anti-CarP) antibodies as potential indicators of disease progression. Additionally, bone turnover markers and specific single nucleotide polymorphisms (SNPs) may influence RA pathogenesis. This study aimed to evaluate the correlation between autoantibody profiles, disease activity, bone turnover markers, and selected SNPs in a cohort of Polish RA patients.

MATERIAL AND METHODS

A total of 138 RA patients from the Department of Rheumatology, Medical University of Lodz, were enrolled. Disease activity was assessed using the Disease Activity Score in 28 joints by C-reactive protein (DAS28-CRP). Serum levels of RF, ACPAs, anti-CarP antibodies, and bone turnover markers (sclerostin, periostin, and Dickkopf-1) were measured using immunoassays. Genotyping for SNPs in PADI4 (rs2240340), STAT4 (rs7574865), and PTPN22 (rs2476601) genes was performed. Patients were categorized into two groups: those positive for anti-CarP antibodies, RF, and ACPA (triple-positive, = 27) and those with other antibody combinations ( = 111).

RESULTS

Demographic characteristics, including age (mean approx. 61 years), gender distribution (approx. 75% female), treatment rates (approx. 75%), and glucocorticosteroid use (approx. 40%), were comparable between groups. The triple-positive group exhibited higher disease activity, with a greater number of painful joints (mean 10.07 vs. 7.72; = 0.017), higher Visual Analogue Scale (VAS) scores for pain (mean 6.26 vs. 5.06; = 0.018), elevated DAS28-CRP scores (mean 4.75 vs. 4.07; = 0.037), and increased erythrocyte sedimentation rate (ESR) (mean 32.92 mm/h vs. 22.82 mm/h; = 0.019). Serologically, the triple-positive group had significantly higher levels of anti-CarP (mean 29.19 ng/ml vs. 16.29 ng/ml; < 0.0001) and ACPAs (mean 395.45 vs. 368.70; < 0.0001), but lower RF levels (mean 164.01 vs. 453.40; = 0.004). Bone turnover markers showed no significant differences between groups, though the difference in sclerostin levels approached statistical significance ( = 0.085), suggesting a possible association of higher bone formation inhibition with triple-positive status. No significant associations were found between the autoantibody profiles and the selected SNPs.

CONCLUSIONS

The presence of anti-CarP antibodies, RF, and ACPA is associated with increased disease activity in RA patients. However, these autoantibody profiles do not significantly correlate with bone turnover markers or the selected genetic polymorphisms in this Polish cohort. Further research is warranted to elucidate the complex interactions between autoantibodies, bone metabolism, and genetic factors in RA.