Plasmatic oxidative stress biomarkers in multiple sclerosis patients with different clinical course

In Multiple Sclerosis (MS) several lines of evidence suggest a major role of oxidative injury in disease progression and Central Nervous System (CNS) tissue damage, although with different mechanisms in the initial and the progressive disease stages. The objective of our study was to compare plasmatic oxidative stress biomarkers levels in patients with Relapsing Remittig (RR) and Secondary Progressive (SP) MS and to correlate biomarkers levels with demographic and clinical variables. We included 30 consecutive patients with RR-MS and 30 with SP-MS, regularly followed-up at six months interval and with annual Magnetic resonance Imaging (MRI). At time of inclusion in the study all patients underwent clinical assessment, including disability, fatigue and sleepiness evaluation and blood sample collection for advanced oxidation protein products (AOPP), plasmatic ferric reducing ability (FRA), a measure of the total antioxidant power o plasma and thiol groups (mainly represented by reduced glutathione, a major non-enzymatic antioxidant) dosage. Results: Plasmatic AOPP, FRA and thiol groups levels were not different in RR and SP and MS patients: however when dividing subjects in “active” (at least one relapse, or MRI evidene of at least one new T2 lesion or gadolinium enhancing lesions during the previous 12 months) and “not active”, we found a significant reduction of FRA levels and thiol groups in the “active” group versus the “not active” (p=0.02 and p=0.04 respectively). No significant correlation was found with demographic and clinical characteristics of patients, including age, disease duration, time interval from the last clinical relapse, disability, fatigue or daytime sleepiness. Conclusions: the ability of plasmatic AOPP, FRA and thiol groups levels to distinguish relapse fro progressive MS seems controversial. However, the total plasmatic antioxidant power and thiol groups seem reduced in patients wih an active disease, independently of the disease stage, thus relating to active CNS inflammation.