Value of ischemia-modified albumin in ankylosing spondylitis

Background/Aim: Ankylosing spondylitis (AS) is a chronic inflammatory illness with a poorly known pathogenesis. Current biomarkers that are used to estimate inflammation are normal in some patients despite having active disease. Recent studies have revealed that oxidative stress may have a role in AS and that there is a close relationship between oxidative stress and inflammation. Ischemia-modified albumin (IMA) is a promising new biomarker for oxidative stress. Thus, the aim of this study was to assess IMA levels and their relationship with disease activity and other inflammatory markers in patients with AS. Methods: This prospective case-control study included 48 patients with AS and 25 healthy controls (HCs). The measured serum levels of IMA, interleukin (IL)-17, and IL-23 were compared between patients with AS and the HC group. We also analyzed the correlation between IMA and disease activity, acute phase reactants, and HLA-B27 positivity. The Ankylosing Spondylitis Disease Activity Score with C-Reactive Protein (ASDAS-CRP) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were used to determine disease activity. Results: There was no difference in serum IMA levels between the AS and HC groups (25.08 [20.49-46.83] vs. 29.89 [29.89-42.0], P=0.146). Only IL-23 was significantly higher in patients with AS (10.81 [7.25-14.06] vs. 7.95 [6.85-10.46], P=0.039). Furthermore, there was no correlation between IMA and IL-23, IL-17, CRP, ESR, BASDAI, or ASDAS-CRP (r=-0.079, P=0.593; r=-0.043, P=0.771; r=-0.018, P=0.906; r=0.047, P=0.751; r=0.281, P=0.053; r=0.162, P=0.271). There was no significant difference between IMA, IL-17, and IL-23 levels in patients with low disease activity (BASDAI <4, ASDAS-CRP <2.1) and high disease activity (BASDAI ≥4, ASDAS-CRP ≥2.1) (BASDAI: P=0.146, P=0.303, P=0.071, and ASDAS-CRP: P=0.451, P=0.410, P=0.324, respectively). There was no difference in IMA levels between HLA-B27-positive patients and HLA-B27-negative patients (P=0.070). Conclusion: Although oxidative stress has been suggested to play a role in AS pathogenesis, we did not find an increase in serum levels of IMA, an oxidative stress biomarker, in patients with AS. Our results suggest that IMA may not be a reliable indicator of inflammation. Further research is needed to determine whether IMA may have a role as a biomarker in AS.