OBJECTIVES: Uric acid (UA), a product of purine metabolism, is known to be reduced in patients with various neurological disorders including multiple sclerosis (MS). However, it has still remained unclear whether there is a close relationship between UA and neuromyelitis optica (NMO). The aim of this study was to investigate the association between serum UA levels and disease activity in NMO. METHODS: Retrospective analysis was made of blood samples during relapses (n = 48) and during stable disease (n = 49) from 20 patients with NMO. As controls, 59 blood samples during relapses from 39 patients with MS and 90 samples from healthy subjects were obtained. Spine magnetic resonance images (MRIs) performed during relapses (n = 24) in NMO were analysed. RESULTS: The results indicated that UA levels during relapses in NMO were significantly lower compared to healthy subjects (P < 0.01), but not different from those during relapses in MS, and that reduced UA levels during relapses in NMO were normalized during stable disease. However, UA levels during relapses were not correlated with Gd enhancement in spine MRI. CONCLUSION: UA levels are associated with clinical disease status in patients with NMO. Further investigations are recommended to elucidate the role of UA as a biomarker of disease activity in NMO.
OBJECTIVES:Uric acid (UA), a product of purine metabolism, is known to be reduced in patients with various neurological disorders including multiple sclerosis (MS). However, it has still remained unclear whether there is a close relationship between UA and neuromyelitis optica (NMO). The aim of this study was to investigate the association between serum UA levels and disease activity in NMO. METHODS: Retrospective analysis was made of blood samples during relapses (n = 48) and during stable disease (n = 49) from 20 patients with NMO. As controls, 59 blood samples during relapses from 39 patients with MS and 90 samples from healthy subjects were obtained. Spine magnetic resonance images (MRIs) performed during relapses (n = 24) in NMO were analysed. RESULTS: The results indicated that UA levels during relapses in NMO were significantly lower compared to healthy subjects (P < 0.01), but not different from those during relapses in MS, and that reduced UA levels during relapses in NMO were normalized during stable disease. However, UA levels during relapses were not correlated with Gd enhancement in spine MRI. CONCLUSION:UA levels are associated with clinical disease status in patients with NMO. Further investigations are recommended to elucidate the role of UA as a biomarker of disease activity in NMO.