Uric acid, which is the final product of purine nucleoside metabolism, is a strong peroxynitrite scavenger. Several studies report on lower serum uric acid levels in multiple sclerosis. In this study, we investigated serum uric acid levels before and after high-dose methylprednisolone treatment (intravenous 1 g/day/5 days) in multiple sclerosis patients. Blood samples from 25 definite multiple sclerosis patients (11 male and 14 female) before and after methylprednisolone treatment (days 0, 6 and 30) and from 20 healthy donors (9 male and 11 female) were analyzed. Serum uric acid levels were measured using a quantitative enzymatic assay (Elitech diagnostics, Sees, France) according to the manufacturer's protocol, and the results were standardized using a commercial uric acid standard solution. We observed significantly increased serum uric acid levels 1 day after the termination of the therapy (day 6). These differences were sustained for 30 days after starting treatment (during remission period). Mean serum uric acid levels were significantly higher in the control group. These results suggest that increasing the uric acid concentration may represent one of the possible mechanisms of action of methylprednisolone in multiple sclerosis.
Oxidative stress and neuroinflammation have a role in the pathogenesis of multiple sclerosis (MS) and in depression. Fatigue is the most disabling symptom in patients with MS and could also be a part of depressive symptomatology. In this study, we measured the serum levels of uric acid (UA) as a marker of oxidative stress and C-reactive protein (CRP) as an inflammatory marker, in 98 patients with MS in relapse and remitting phase of illness and 35 healthy subjects. Degree of depressive symptomatology and fatigue were assessed with Beck's Depression Inventory (BDI) and Fatigue Severity Scale (FSS). Further, we examined the possible correlation of these biomarkers with symptoms of depression and fatigue. Relapse and remitting MS had a lower serum UA levels than controls (236.97 ± 9.25 µmol/L vs. 268.27 ± 0.09 µmol/L vs. 314.82 ± 11.02 µmol/L; p = 0.000), while sera levels of CRP were higher in relapse than remitting patients (4.46 ± 0.40 mg/L vs. 1.01 ± 0.38 mg/L; p = 0.000). Patients in relapse had higher BDI scores (15.68 ± 16.62 vs. 8.36 ± 7.10; p = 0.045). Decreased UA levels showed weak negative correlation with the presence of sadness and disturbed daily activities, higher CRP levels positively correlated with severe depression and the correlation between depression and fatigue was also observed (p < 0.05). It is possible that decreased UA levels lead to sadness, disturbed daily activities and severe disability. Every attack of CRP elevation in relapse could additionally precipitate the depression onset. The clinicians must pay special attention to early detection of fatigue because it could precede depression and improve further treatment.
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