Elevated Apolipoprotein A1 and HDL Cholesterol Associated with Age-related Macular Degeneration: 2 Population Cohorts

Publikation: Bidrag til tidsskriftTidsskriftartikelfagfællebedømt

CONTEXT: To enable prevention and treatment of age-related macular degeneration (AMD), understanding risk factors for AMD is important. OBJECTIVE: We tested the hypotheses that elevated plasma apolipoprotein A1 and high-density lipoprotein (HDL) cholesterol and low levels of low-density lipoprotein (LDL) cholesterol are associated with increased risk of AMD. METHODS: From the Danish general population, we studied 106 703 and 16 032 individuals in the Copenhagen General Population Study (CGPS) and the Copenhagen City Heart Study (CCHS) with median follow-up of 9 and 32 years, respectively.The main outcome measures were 1787 AMD in CGPS and 206 in CCHS. RESULTS: Higher concentrations of plasma apolipoprotein A1 and HDL cholesterol, and lower concentrations of LDL cholesterol, were associated with higher risk of AMD in CGPS. After multifactorial adjustment, individuals in the highest versus lowest quartile of plasma apolipoprotein A1 and HDL cholesterol had hazard ratios for AMD of 1.40 (95% CI: 1.20-1.63) and 1.22 (1.03-1.45). Corresponding hazard ratios for individuals in the lowest versus highest quartile of LDL cholesterol were 1.18 (1.02-1.37). Per 100 mg/dL higher plasma apolipoprotein A1, 1 mmol/L (39 mg/dL) higher HDL, and 1 mmol/L (39 mmol/L) lower LDL cholesterol, the hazard ratios for AMD were 1.53(1.31-1.80), 1.19 (1.07-1.32), and 1.05 (1.00-1.11), respectively, with similar results across strata of different risk factors. Higher concentrations of HDL cholesterol were also associated with higher risk of AMD in the CCHS. CONCLUSION: Elevated plasma apolipoprotein A1 and HDL cholesterol and lower LDL cholesterol are associated with increased risk of AMD.

OriginalsprogEngelsk
TidsskriftThe Journal of clinical endocrinology and metabolism
Vol/bind106
Udgave nummer7
Sider (fra-til)e2749-e2758
Antal sider10
ISSN0021-972X
DOI
StatusUdgivet - 16 jun. 2021

Bibliografisk note

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© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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