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A Method of Trigonometric Modelling of Seasonal Variation Demonstrated with Multiple Sclerosis Relapse Data
Published on: December 9, 2015
Coordinated oxidative shift during relapse and recovery in multiple sclerosis: A paired analysis of multiple
Caner Baydar1, Abdullah Yılgör1
1Department of Neurology, Van Yüzüncü Yıl University Faculty of Medicine, Van, Turkey.
Background:
Oxidative stress plays a central role in the pathogenesis of multiple sclerosis (MS), contributing to inflammation, demyelination, and neurodegeneration. Acute relapse periods may represent a critical phase characterized by intensified oxidative imbalance; however, comprehensive evaluation of multiple oxidative pathways during relapse remains limited.
Objective:
To investigate dynamic changes in oxidative stress markers in patients with MS during relapse and after clinical recovery.
Methods:
Fifty patients with relapsing-remitting MS were evaluated during relapse and one month after clinical recovery. Blood samples were obtained prior to corticosteroid treatment. Ischemia-modified albumin (IMA), asymmetric dimethylarginine (ADMA), total sulfhydryl groups (TSH), and protein carbonyl (PC) levels were measured. Paired comparisons between relapse and post-relapse periods were performed, and results were additionally compared with 50 age- and sex-matched healthy controls. Correlation analyses with Expanded Disability Status Scale (EDSS) scores, effect size analyses, and sensitivity analyses according to disease-modifying therapy categories were also conducted.
Results:
All oxidative stress markers showed significant changes across study groups. IMA, ADMA, and PC levels were significantly elevated during relapse compared with both post-relapse and control groups (p < 0.001 for all comparisons). Although these markers significantly decreased following clinical recovery, they remained higher than control levels. TSH levels were significantly increased during relapse, suggesting a compensatory antioxidant response. Paired analyses demonstrated a significant reduction in all markers following clinical recovery, with large effect sizes observed across oxidative stress parameters. Sensitivity analyses showed that the overall relapse-associated oxidative profile remained largely consistent across disease-modifying therapy categories. Exploratory Spearman correlation analyses demonstrated weak-to-moderate positive correlations between ADMA and TSH levels and EDSS scores.
Conclusion:
MS relapse is associated with a broad but partially reversible oxidative stress response involving ischemia-related, endothelial dysfunction-associated, antioxidant, and protein oxidation pathways. The observed biomarker changes support the presence of a relapse-associated redox imbalance linked to acute inflammatory activity in MS.
