Clin Exp Ophthalmol. 2022 Feb 26. doi: 10.1111/ceo.14067. Online ahead of print.
ABSTRACT
BACKGROUND: This study aimed to examine possible causal associations between various components of metabolic syndrome and glaucoma-related phenotypes.
METHODS: A two-sample Mendelian randomization study was conducted with the models of IVW, maximum likelihood, weighted median, and MR-Egger regression. We accessed data from publicly available genome-wide association studies for individual parameters of metabolic syndrome as the exposures and the data for glaucoma and its endophenotypes as the outcomes.
RESULTS: Among eleven exposures and six outcomes examined in this Mendelian randomization study, only fasting blood glucose level showed evidence of a causal influence on intraocular pressure. Results analyzed by the inverse-variance weighted model suggested that each one-SD increase in genetically predicted fasting blood glucose level was significantly associated with 0.80 SD elevation in intraocular pressure (β: 0.80, 95%CI: 0.38-1.22, P: 2.12e-4). The maximum likelihood model (β: 0.82, 95%CI: 0.39-1.25, P:1.616e-4) also supported a significant causal effect. The weighted median model (β: 0.78，95%CI: 0.17-1.39, P: 0.012) showed a nominally significant effect whereas the MR-Egger model (β: 0.63, 95%CI: -0.32-1.59, P: 0.212) showed a consistent direction of effect but was not statistically significant. Several sensitivity analyses indicated no evidence of directional horizontal pleiotropy that would bias the result.
CONCLUSIONS: This Mendelian randomization study provides evidence for a causal role for genetically determined higher fasting blood glucose level in the development of increased intraocular pressure. This finding could be considered in the monitoring and control of intraocular pressure and may be instrumental in prevention strategies for ocular hypertension.
PMID:35218584 | DOI:10.1111/ceo.14067
