URIC ACID LEVELS IN SERUM AND CSF OF ALS PATIENTS

Objective: Urate (UA) is a potent antioxidant that effectively scavenges reactive nitrogen and oxygen radicals, and persons with a high plasma UA level may be at lower risk of some neurodegenerative disorders, as Parkinson’s disease (PD). Low plasma UA level has been observed in Alzheimer’s disease (AD) and vascular dementia, but there is no data on correlations to neuropsychological test results in these patient groups. Amyotrophic Lateral Sclerosis (ALS) is a devastating motor neuron disease, with a highly variable rate of progression and whose diagnosis is chiefly based on clinical and neurophysiological parameters. The etiopathogenesis is unknown, but the oxidative stress seems to play an important role. As UA works as an antioxidant, and given the phenotypic heterogeneity of the disorder (in terms of site of onset and clinical progression), we asked whether UA could represent a biological marker in ALS. Therefore, in the present study we assayed UA in the CSF and serum of ALS patients and disease controls, and evaluated its relationship with different clinical variables and the rate of progression. Patients: 146 ALS patients (M/F 1.8; mean age at onset 61± 11.65 years; 41 with bulbar onset, 35%) who met the Revised El Escorial criteria for clinically definite, probable or probable with laboratory support were selected. General demographic and clinical features of this cohort were recorded. Controls were 141 patients admitted in our hospital for suspected neurological disorders such as multiple sclerosis, myelitis and polyneuropathy. CSF and serum from ALS patients and disease controls was obtained as a necessary step of the diagnostic work-up and all patients gave an informed consent to the procedure. Methods: CSF and serum were obtained from fasted patients and aliquots stored at –80°C until use. UA level in CSF and serum was assaying using a colorimeter enzymatic test (UA plus, COBAS ®). Results: The median serum level of UA (mg/dl) was 4.65 (3.6-5.6) in the ALS patients and 4.80 (3.9-5.6) in controls (p=ns). Further, UA CSF levels (mg/dl) were no significantly different between ALS and controls (ALS, 0.3 [0.2-0.4] vs controls, 0.28 [0.2-0.4], p=ns). CSF and serum UA in ALS was nor related to the severity of the disease (as measured as a rate of progression with the clinimetric Appel ALS rating scale), respiratory function, age at onset and site of onset. Conclusion: UA is not a biochemical marker in ALS and is probably unrelated to its pathophysiology