Abstract
Objective: To explore the associations between serum uric acid levels with survival in male and female ALS patients.Methods: A longitudinal cohort study was carried out including 313 sporadic and 16 familial ALS patients with repeated serum uric acid measurements. Multivariate Cox regression models were used to evaluate the survival-related factors.Results: There were 207 male and 122 female, and the mean age of onset was 55.7 ± 11.2 years old. The male patients had significantly higher baseline uric acid levels than that in female patients (342.4 ± 91.4 vs. 279.3 ± 71.4 μmol/L; p < 0.0001). The uric acid levels were inversely associated with the decline rate of ALSFRS-R per month (ΔALSFRS-R). After multivariate Cox regression analysis, a survival advantage was found in male, but not female, with higher serum uric acid levels. In males, a shorter diagnostic delay (≤10 m), lower BMI at baseline (≤18.70 kg/m2), faster disease progression (ΔALSFRS-R > 0.63), and lower baseline uric acid levels (≤292 μmol/L, HR: 1.936; 95% CI: 1.334–2.810) were associated with a shorter survival. During follow-up, the serum uric acid levels were not significantly altered over time.Conclusion: There is an inverse correlation between baseline serum uric acid levels and risk of death, prominently in male ALS patients.
Highlights
Amyotrophic lateral sclerosis (ALS) is a chronic and incurable adult-onset neurodegenerative disorder that primarily impairs upper and lower motor neurons [1]
After plasma component analysis using surface enhanced Raman spectroscopy, we further found that the ALS patients with short duration showed a significantly decreased antioxidant level, and the metabolism of glutathione was correlated with the disease progression [17]
1 case combined with chronic reduction of renal function, and 8 cases combined with cancers (1 with hepatic carcinoma, 1 with nasopharyngeal carcinoma, 1 with glioma, 2 with breast cancer, 2 with lung cancer, and 1 with rectal cancer)
Summary
Amyotrophic lateral sclerosis (ALS) is a chronic and incurable adult-onset neurodegenerative disorder that primarily impairs upper and lower motor neurons [1]. It is characterized by male predominance, upper limb onset, relentlessly progressive muscle weakness and atrophy, and a variable natural history [2]. Pathophysiological mechanisms that contribute to the development and progression of ALS are complicated, including dysfunction of RNA metabolism, impaired proteostasis, impaired DNA repair, mitochondrial dysfunction and oxidative stress, axonal transport defects, glutamate excitotoxicity, and neuroinflammation [4]. Increasing evidence supports that oxidative stress may play a critical role in the pathogenesis of ALS, the SOD1
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