Correlation of the Disease Activity and Pro-inflammatory Cytokine Expression Between Young and Elderly Onset Rheumatoid Arthritis

Abstract

Background and Aims: Rheumatoid arthritis (RA) is a complex autoimmune inflammatory disease-causing disability. The immunopathogenic difference between elderly onset RA (EORA) and younger-onset RA (YORA) and the factors responsible for their clinical characteristics are yet to be explored completely. The study was done to correlate inflammatory biomarkers in EORA patients and compare with YORA patients. Methods: A cross-sectional study comprising 30 patients each for YORA and EORA was done. Serum levels of interleukin IL-1β, IL-6, IL-8, tumour necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and anticyclic citrullinated peptide were determined by Enzyme-Linked Immunosorbent Assay (ELISA). These were correlated with disease activity using the DAS28, and the modified Larson score was used to assess bone erosion. Results: Significantly higher levels of serum IL-6 (25.1 vs. 12.8 pg/mL) and IL-8 (83.5 vs. 65.15 pg/mL) were found in EORA patients, while significantly higher levels of serum TNF-α (360.8 vs. 86.3 pg/mL) were found in patients with YORA. IL-1β, IL-8 and TNF-α have a significantly positive correlation with DAS28 in YORA, while IL-1β, TNF-α and IFN-γ are significantly associated with disease activity in EORA. Increased bone erosion was linked to EORA. Conclusion: Apart from clinical symptoms, serological profile, EORA, and YORA have a distinct cytokines profile. This provides a valuable insight for selecting targeted therapies, especially in managing naive and refractory RA cases of EORA. Given the higher risk of joint damage in EORA, early and aggressive management may result in early remission and improve patient’s quality of life. © 2025 The Author(s). This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).