The effect of anti-TNF agent on oxidation status in patients with ankylosing spondylitis.
The aim of this study was to comparatively evaluate oxidative status of ankylosing spondylitis (AS) patients receiving anti-tumor necrosis factor (TNF) or non-steroid anti-inflammatory drugs (NSAID). Forty-seven patients with AS and 27 healthy controls were enrolled. Of these, 23 were on anti-TNF (group 1) and 24 on NSAIDs (group 2). Groups 1 and 2 were consisted of matched patients with respect to age, gender, body mass index, disease duration, C-reactive protein, erythrocyte sedimentation rate, total cholesterol, and Bath Ankylosing Spondylitis Disease Activity Index. Mean duration of treatment for patients in group 1 was 12.6 +/- 6.8 months. Serum total antioxidative status (TAS) and total oxidative status (TOS) levels were determined using new automated methods. Oxidative stress index (OSI) was calculated. The groups' carotid intima-media thicknesses (IMT-C) were also measured using ultrasonography. Group 1 had the highest TAS and lowest TOS levels. The TOS levels of group 1 was lower than the control, while group 2 being higher than controls. The difference in TOS levels between group 1 and group 2 was statistically significant (p = 0.040). OSI values were highest in group 2 and lowest in group 1. There was no significant correlation between oxidant/antioxidant parameters and IMT-C for group 1 (r = -0.30, p = 0.198 for OSI; r = 0.22, p = 0.366 for TAS; r = -0.22, p = 0.361 for TOS). This is the first study to evaluate total oxidative/antioxidative status in patients with AS on anti-TNF agent. These results clearly indicate positive effects of anti-TNF treatment on oxidative status of AS patients. The limited effects of NSAIDs compared with controls may be due to excess impaired oxidative status in the patients in this study.
Karkucak
Murat
M
Department of Physical Medicine and Rehabilitation, Farabi Hospital, Karadeniz Technical University, Medical School, 61080, Trabzon, Turkey. muratkarkucak@yahoo.com
Capkin
Erhan
E
Alver
Ahmet
A
Akyuz
Ayse
A
Kiris
Abdulkadir
A
Ak
Emel
E
Topbas
Murat
M
Tosun
Mehmet
M
D000068879:Adalimumab; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects* / Q000276:immunology; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept