Glaucoma, a leading cause of irreversible blindness worldwide, is a silent thief of sight. With over 110 million people predicted to be affected by glaucoma by 2040, early detection and treatment are crucial. However, glaucoma often progresses silently in its early stages, making it challenging to diagnose. Intraocular pressure (IOP) measurement is a key aspect of glaucoma diagnosis, but some patients with glaucoma exhibit normal IOP levels, suggesting the involvement of other factors. Recent research has explored the potential role of uric acid (UA) in glaucoma development and its potential as a biomarker.
A meta-analysis conducted by researchers from multiple institutions aimed to evaluate the association between serum UA levels and glaucoma. The analysis included six case-control studies involving a total of 1,221 glaucoma patients and 1,342 control subjects. The results indicated that glaucoma patients tend to have higher serum UA levels compared to control subjects, although the difference was not statistically significant. The high level of heterogeneity among the studies suggests considerable variation in the results.
Glaucoma is a complex condition with various theories and contributing factors. Oxidative stress and neuroinflammation are believed to play a significant role in glaucomatous optic neuropathy. Antioxidants, including UA, have shown potential protective effects in glaucoma. However, systemic inflammation and bacterial infections have also been associated with glaucomatous damage. There may be an imbalance between antioxidative and oxidative processes in glaucoma patients. Additionally, elevated UA levels in the aqueous humor of some glaucoma patients suggest a potential role in trabecular meshwork dysfunction and elevated IOP.
It is important to note that elevated IOP alone does not fully explain glaucoma pathophysiology. Other risk factors, such as vascular impairment and endothelial dysfunction, have been suggested. UA-induced inflammatory responses and oxidative stress can contribute to microvascular impairments, potentially affecting the retinal microvasculature. Chronic renal disease, which is associated with elevated UA levels, has also been significantly linked to an increased risk of developing glaucoma.
While the meta-analysis does not establish a causal relationship between UA and glaucoma, it highlights the need for further research into the potential role of UA as a biomarker in glaucoma research. Detecting glaucoma early remains a challenge due to its asymptomatic nature, and additional biomarkers could aid in early diagnosis and treatment. Further studies exploring the relationship between UA and glaucoma may provide valuable insights into the pathogenesis of this sight-stealing condition.