Abstract
Background
Normal tension glaucoma (NTG) is a common subtype of glaucoma that progresses silently and can lead to irreversible vision loss if left untreated. Emerging evidence suggests that inflammation and vascular dysfunction may play a role in its pathogenesis. C-reactive protein (CRP), a marker of systemic inflammation and atherosclerosis, has been widely studied as a prognostic indicator in various diseases. However, its potential association with NTG remains unclear. This meta-analysis aims to clarify the relationship between CRP levels in individuals with NTG compared to those without the condition.
Methods
We systematically searched PubMed, Embase, and Scopus for observational studies published up to 31 October 2023 investigating CRP levels in NTG patients and controls. Study quality and risk of bias were evaluated using the Newcastle–Ottawa Scale. Eligible studies reporting CRP levels were analyzed using standardized mean differences (SMDs) and 95% confidence intervals (CIs).
Results
A meta-analysis of ten case-control studies involving 766 patients revealed that CRP levels were significantly higher in the NTG group compared to controls (SMD: 0.731, 95% CI: 0.147–1.316 ; z = 2.454; P = 0.014). However, no significant difference in CRP levels was observed between the POAG group and controls (SMD = 0.093; 95% CI: −0.160–0.345; z = 0.719; P = 0.472).
Conclusion
Elevated circulating CRP levels were significantly associated with NTG, suggesting a potential systemic inflammatory contribution to its pathogenesis. Although CRP may serve as an adjunctive marker for identifying high-risk individuals, its clinical value remains provisional and requires confirmation in future prospective studies.
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
