A metaanalysis shows that levels of an antioxidative endogenous metabolic byproduct-uric acid-are correlated with disease activity in multiple sclerosis.
A metaanalysis shows that levels of an antioxidative endogenous metabolic byproduct—uric acid—are correlated with disease activity in multiple sclerosis.
In a study published in the journal Clinical Chemistry and Laboratory Medicine on September 20, 2014, investigators Moccia et al identified uric acid as a potential biomarker in the progression of multiple sclerosis (MS) disability.1
Uric acid, which has activity as a natural scavenger of oxygen radicals, is present in the bloodstream as a breakdown product of purines (adenine and guanine). In previous animal studies, uric acid has been shown to have some potential as a treatment for MS.1
Results of these studies led investigators in the present study to search for a relationship between MS severity and levels of uric acid. In the case-control study using propensity score matching, investigators paired 362 patients with MS to 181 control individuals without MS.1
To reduce variation between populations, investigators corrected data for patient age, gender, and kidney function. Upon regression analysis, investigators identified a significant association between low levels of serum uric acid among patients with MS compared with controls, with an R-squared value of 30.4% and statistical significance for the correlation (P = .014).1
Lower levels of uric acid were associated with a longer disease duration, a longer duration since diagnosis, and higher Expanded Disability Status Scale (EDSS) scores (P <.001, all comparisons). These findings suggest that uric acid may be a biomarker of MS disability and progression, although past studies reveal that uric acid may have a limited role as a marker of treatment response or as a therapeutic target in MS.1
For instance, a 2006 analysis published in the journal Clinical Neurology and Neurosurgery, found that uric acid levels did not change as a result of immunomodulatory or immunosuppressive drug treatment among patients with MS.2
Additionally, in the Association of Inosine and Interferon beta in relapsing-remitting Multiple Sclerosis (ASIIMS) trial, investigators administered a precursor of uric acid—inosine—to patients with MS in conjunction with interferon-beta over the course of 2 years. The results of this trial were negative and uric acid did not have any additional benefit on disability outcomes versus interferon-beta alone.3
In spite of the negative result of the ASIIMS trial, antioxidative drugs may still have a future in treatment of multiple sclerosis. However, uric acid may be a biomarker—not a treatment modality. Studying uric acid may help physicians predict the progression of multiple sclerosis in patients, although previous research shows that uric acid levels do not predict response to treatment2 and supplementation with uric acid does not alter the progression of disability in MS.3
Further study will be necessary to determine whether or not drugs that mimic the effects of uric acid are of any therapeutic value in patients with MS.