Should we be treating MS with anti-oxidants? #MSBlog #MSResearch
"It has been known for sometime that uric acid is a weak anti-oxidant and is reduced in condition associated with the production of oxygen free radicals. In Parkinson's disease low uric acid levels are associated with a poor outcome. This study although small hints at a similar observation in MS. The findings clearly needs to be confirmed, but the study hints at a potential biomarker that can be included in longitudinal studies of outcome in MS. Based on this study it appears that uric acid is unlikely to be useful in individual MSers, but could be used for hypothesis testing in large groups of subjects. I would be very interested to know if DMTs affect uric acid levels and whether of not UA levels correlate with disease activity. I would predict that MSers with NEDA would have higher levels than those with ongoing disease activity. This study also shows that MS is a systemic disease and affects metabolism in general; another reasons for us to take a systems biology approach to the disease when thinking about it. For those of you who don't know about uric acid; it is a breakdown product of DNA metabolism and is excreted in the urine. Too much uric acid can lead to gout. I wonder if MSers are lower risk of getting gout?"
Background: Uric acid (UA) is reduced in MS, and possibly relates to MS outcomes, with lower UA levels in subjects experiencing a relapse or presenting higher disability scores.
Methods: The present retrospective longitudinal study evaluated UA variations in MS, in relation to clinical relapses, disability progression, and cognitive functions. We included 141 subjects with relapsing-remitting MS (RRMS) and performed expanded disability status scale (EDSS), symbol digit modalities test (SDMT) and UA evaluation at baseline visit and after 2-year follow-up.
Results: Paired t test showed significantly lower UA levels after 2-year follow-up than at baseline (3.987 ± 1.135 and 4.167 ± 1.207 mg/dL, respectively) (p = 0.001). The difference in UA levels between 2-year follow-up and baseline related to EDSS sustained progression (p < 0.001; OR = 0.099), and presented a trend for clinical relapses at logistic regression (p = 0.211; OR = 0.711) and for the time to relapse at Cox regression (p = 0.236; HR = 0.792). Analysis of variance showed reduced baseline UA levels in subjects with impaired SDMT at baseline (p = 0.045; adjusted R 2 = 0.473) and after 2-year follow-up (p = 0.034; adjusted R 2 = 0.470).
Conclusion: This is the first study showing a progressive reduction of UA levels during the course of RRMS, suggesting a progressive decrease of antioxidant reserves, in relation to relapse risk, disability progression and cognitive function.