Abstract
Uric acid (UA) is a major antioxidant molecule and has been hypothesized to have a protective effect on the central nervous system against oxidative damage. We prospectively investigated the serum concentration of UA in primary angle closure glaucoma (PACG), and explored the association between serum concentration of UA and the severity of PACG. Using a retrospective case-control study design, 886 PACG subjects and 994 control subjects who attended the Eye & ENT Hospital of Fudan University, were eligible for this study. Glaucoma severity was classified as mild (MD ≤ 6.00 dB), moderate (12 dB ≥ MD > 6 dB) and severe (MD > 12 dB) based on the MD (mean deviation). The levels of UA were significantly lower (p = 0.025) in PACG (0.286 ± 0.082 mmol/l) compared with control (0.295 ± 0.085 mmol/l). The mean serum UA levels were lowest in the severe group (0.281 ± 0.074 mmol/l) followed by moderate (0.282 ± 0.080 mmol/l) and mild (0.297 ± 0.090 mmol/l) with significant differences among the three groups (p = 0.032). In multivariate regression analysis, there was a significant negative correlation between UA level and vertical cup-disc ratio (B = −0.165, p = 0.035). Significantly lower serum UA concentration in PACG and its negative association with disease severity presented it as an important candidate in reaction to oxidative stress in glaucoma pathogenesis.
Highlights
Primary glaucoma is a progressive optic neuropathy and one of the leading causes of global irreversible blindness, and the number of people with glaucoma worldwide is projected to increase from 76.0 million in 2020 and 111.8 million in 2040 [1,2,3]
The mean serum levels of Uric acid (UA) and uric acid/creatinine (UA/Cr) ratio were significantly lower in the primary angle closure glaucoma (PACG) compared with the control group (p < 0.001)
To the best of our knowledge, this study has been the first to focus on the investigation of serum UA and UA/Cr ratios in PACG and further evaluate their relationship with disease severity
Summary
Primary glaucoma is a progressive optic neuropathy and one of the leading causes of global irreversible blindness, and the number of people (aged 40–80 years) with glaucoma worldwide is projected to increase from 76.0 million in 2020 and 111.8 million in 2040 [1,2,3]. Whether serum UA levels are changed and involved in the pathophysiological mechanisms of PACG remained unclear. Babizhayev MA et al [21] reported that prevention of oxidative stress exposure to the trabecular meshwork with a N-acetylcarnosine ophthalmic prodrug of carnosine and oral formulation of nonhydrolizedcarnosine may help to reduce the progression of glaucoma. Several studies suggested that www.impactjournals.com/oncotarget markers of oxidative stress including chemia-modified albumin, protein nitrotyrosine, lipid oxidation products and 8-hydroxydeoxyguanosin, increased significantly in glaucoma [7, 22,23,24,25]. Whether peripheral blood UA concentration and UA/Cr ratio were changed in PACG and associated with the pathogenesis of glaucoma still remained to be studied
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