Findings indicate that MetS may serve as a valuable marker for the secondary prevention of RAO, and stringent management of hyperglycemia and hypertension could contribute to a reduced risk of RAO.
Abstract
Purpose
To examine the association between MetS, its five components (central obesity, hypertension, hyperglycemia, dyslipidemia, and hypertriglyceridemia) and RAO, and to assess whether genetic susceptibility to key components of the MetS (hypertension, hyperglycemia) interacts with these associations.
Methods
Based on the UK Biobank, Cox proportional hazards regression models were applied to assess the associations between MetS, its individual components, and the incidence of RAO. Restricted cubic spline analysis was applied to determine non-linear trends in their associations. Polygenic risk scores of hypertension and diabetes were further used to assess the genetic interactions of MetS components with RAO.
Results
A total of 361,578 participants with a mean age of 55.94 years were included in the analysis. The risk of RAO was significantly higher in individuals with MetS (HR: 1.59, 95% CI: 1.05-2.42), as well as in those with its key components: hypertension (HR: 3.06, 95% CI: 1.52-6.16) and hyperglycemia (HR: 2.70, 95% CI: 1.27-3.83). Genetic analysis revealed that MetS was associated with a significantly increased risk of RAO in individuals with a higher genetic predisposition to T2DM (HR: 3.20, 95% CI: 2.23-4.17).
Conclusions
MetS, especially its key components hypertension and hyperglycemia, increased the risks of RAO onset. Genetic susceptibility to T2DM also increased RAO risk in MetS patients. These findings indicate that MetS may serve as a valuable marker for the secondary prevention of RAO, and stringent management of hyperglycemia and hypertension could contribute to a reduced risk of RAO.
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BACKGROUND
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METHODS
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