Tumour necrosis factor-α, interleukin-2 soluble receptor and different inflammatory parameters in patients with rheumatoid arthritis

• Published in: Mediators of Inflammation Vol. 2002; no. 6; pp. 345 - 349
• Main Authors: Fröde, Tânia Silvia, Tenconi, Patrícia, Debiasi, Marilei Reynaud, Medeiros, Yara Santos
• Format: Journal Article
• Language: English
• Published: United States Hindawi Limiteds 01-12-2002; Hindawi Limited
• Subjects: Adolescent; Arthritis, Rheumatoid - blood; Arthritis, Rheumatoid - metabolism; beta 2-Microglobulin - analysis; Blood Sedimentation; C-Reactive Protein - analysis; Case-Control Studies; Child; Female; Humans; Male; Receptors, Interleukin-2 - metabolism; Solubility; Tumor Necrosis Factor-alpha - metabolism; C-reactive protein; Erythrocyte sedimentation rate; Cytokines; Rheumatoid arthritis; β2-Microglobulin
• ISSN: 0962-9351; 1466-1861
• DOI: 10.1080/0962935021000051539

BACKGROUND and aims: Although the participation of cytokines in the pathogenesis of rheumatoid arthritis (RA) seems to be unequivocal, their relationship with current serum markers of this disease is not clear. The present study analyses whether there is any correlation between the levels of tumour necrosis factor-a (TNF-α), interlukin-2 soluble receptor (sIL-2R) and the concentrations of C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) and β2-microglobulin in a group of 21 patients with RA, all rheumatoid factor positive. Methods: The levels of TNF-a and sIL-2R were analysed in association with other parameters of inflammation (ESR, CRP and β2-microglobulin). Results: In comparison with the control group, RA patients presented high median levels of both cytokines, TNF-α (6.4 pg/ml) and sIL-2R (56 pmol/L), as well as of ESR (34mm/h), CRP (0.9mg/dl) and β2-microglobulin (1.6mg/dl) (p ＜ 0.01). However, only ESR levels in the RA group significantly differ from the control group (p ＜ 0.01). No correlation was found between the inflammatory parameters. Conclusions: These results suggested that TNF-α and slL-2R levels are up-regulated in RA patients but did not significantly differ from the control group. Due to the chronic course of this disease, other inflammatory markers must be identified in order to provide early therapeutic strategies to these patients.