Rheumatoid arthritis (RA) is a common chronic inflammatory and autoimmune disease primarily involving the synovial membranes and articular structures of multiple joints, although with unknown etiology .
In regulating inflammation and immunity, a vast network of interacting cells and cytokines is required. The endocrine system also participates in various ways in immune regulation through the actions of growth hormones, especially insulin-like growth factor-1 (IGF-1) . IGF-1 promotes the growth and differentiation of the bone and cartilage tissue and participates in regulating immunity and inflammation .
IGF-1 has a fundamental role in both prenatal and postnatal development; it binds to the IGF-1 receptor (IGF-1R) to exert all of its known physiologic effects, which are modulated by multiple IGF-binding proteins (IGFBPs) . Currently, six IGFBP types have been identified (IGFBP-1 to IGFBP-6). Among them, IGFBP-3 is the most important, and it carries up to 75 to 90% of circulating IGF-1 and regulates the action of IGF-1 through interaction with the receptor IGF-1R . Several rheumatic diseases, such as osteoarthritis, diffuse idiopathic skeletal hyperostosis, and RA, exhibit abnormalities in the serum and/or synovial fluid levels of growth hormone (GH)/IGF-1 [3, 6, 7]. However, the mechanism on how the IGF system is involved in RA disease activity remains poorly known. Our previous study showed that the IGFBP-3 levels were significantly higher in patients with RA, particularly in those with active RA. Furthermore, the IGFBP-3 levels in the serum and synovial fluid had a significantly positive correlation with the erythrocyte sedimentation rate (ESR) and CRP level that highly correlate with RA disease activity in patients with RA .
However, the serum concentration of IGFBP-3 either increases [9, 10] or decreases , depending on the results presented in the previous studies, presumably because of differences in the patient’s age or RA activity level.
Therefore, this study aimed to determine the relationship between the IGFBP-3 system and the disease activity of RA and to reproduce the results of our previous study.