Elevated serum interleukin-23 levels in ankylosing spondylitis patients and the relationship with disease activity

• Published in: Nagoya journal of medical science Vol. 77; no. 4; pp. 621 - 627
• Main Authors: Ugur, Mahir, Baygutalp, Nurcan Kilic, Melikoglu, Meltem Alkan, Baygutalp, Fatih, Altas, Elif Umay, Seferoglu, Buminhan
• Format: Journal Article
• Language: English
• Published: Japan Nagoya University 01.11.2015
• Subjects: Original Paper; disease activity; ankylosing spondylitis; interleukin-23
• ISSN: 0027-7622; 2186-3326

This study was aimed to evaluate the relationship between serum interleukin-23 (IL-23) levels and ankylosing spondylitis (AS).Twenty male patients diagnosed with ankylosing spondylitis according to the 1984 modified New York criteria for AS and twenty male healthy controls were included in this study.The demographic characteristics, clinical and laboratory findings of the patients were recorded. Serum IL-23 levels, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) were measured in both the AS and control groups. The Bath ankylosing spondylitis disease activity ındex (BASDAI), the Bath ankylosing spondylitis functional index (BASFI), and the Bath ankylosing spondylitis metrology index (BASMI) were evaluated as disease activity parameters. The AS patients were divided into two subgroups as active and inactive in respect of CRP, ESR levels and BASDAI scores. The mean serum IL-23 levels of the AS and control groups were 334.45±176.54 pg/ml and 166.49±177.50 pg/ml respectively, and there was a significant difference between the groups. Correlation analysis of serum IL-23 levels with clinical and laboratory parameters showed that there were positive correlations between serum IL-23 levels and the BASDAI, BASFI scores in total, active and inactive patients and the BASMI scores in total and inactive patients and negative correlations between serum IL-23 levels and ESR in inactive patients. It was shown that altered serum IL-23 levels were related to AS disease activity. Further studies in large patient series are necessary to investigate the role of IL-23 protein in etiopathogenesis of AS.