Abstract

Introduction and objectivesThe etiopathogenesis of ankylosing spondylitis (AS), which is a chronic, progressive, inflammatory, systemic disease, has not been fully elucidated yet. Thiol-disulfide homeostasis, a component of antioxidant defense, is thought to play a role in the etiology of inflammatory diseases. We aimed to evaluate the existence of oxidative stress in active AS patients with thiol-disulfide homeostasis. Materials and methodsPatients who were found to have high (n: 27) and very-high (n: 18) activity levels with ASDAS-ESR and 40 healthy controls participated in the study. Serum native-thiol (NT), total-thiol (TT), and disulfide levels were analyzed by an automated colorimetric method. ResultsWhile TT and NT levels were significantly decreased in patients compared to the control group, the disulfide levels were increased. There was a significant negative correlation between ESR, and NT, TT in both groups and also between hsCRP and NT, TT in very-high active AS patients.TT and NT levels were significantly higher in the nonsteroidal anti-inflammatory drug (NSAID) users compared to those using biological agents. ConclusionsThe deterioration of thiol-disulfide homeostasis in favor of disulfide; correlations between ESR, CRP, and NT, TT support the use of thiol-disulfide variables in determining the disease activity level.

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