Lipids, lipid genes, and incident age-related macular degeneration: the three continent age-related macular degeneration consortium.

Lipids, lipid genes, and incident age-related macular degeneration: the three continent age-related macular degeneration consortium.
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DOI:
10.1016/j.ajo.2014.05.027
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发表时间:
2014-09
影响因子:
4.2
通讯作者:
Wang, Jie Jin
Wang, Jie Jin
中科院分区:
医学1区
文献类型:
--
作者:
Klein, Ronald;Myers, Chelsea E.;Buitendijk, Gabrielle H. S.;Rochtchina, Elena;Gao, Xiaoyi;de Jong, Paulus T. V. M.;Sivakumaran, Theru A.;Burlutsky, George;McKean-Cowdin, Roberta;Hofman, Albert;Iyengar, Sudha K.;Lee, Kristine E.;Stricker, Bruno H.;Vingerling, Johannes R.;Mitchell, Paul;Klein, Barbara E. K.;Klaver, Caroline C. W.;Wang, Jie Jin

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描述血脂水平和脂质通路基因与年龄相关性黄斑变性(AMD)发病率的关系。荟萃分析.三个基于人口的群组。来自比弗坝眼科研究(BDES)、蓝山眼科研究(BMES)和鹿特丹研究(RS)的6950名参与者。参与者被跟踪了20多年,每隔5年进行一次检查。使用随机效应反向加权荟萃分析模型计算与高于平均值的每个标准差的脂质水平相关的风险比(HR),或与每个脂质途径基因的每个额外风险等位基因相关的风险比(HR),并对已知的AMD风险因素进行调整。AMD的发病率。在BDES、BMES和RS中,早期AMD的平均5年发病率分别为8.1%、15.1%和13.0%。将这三项研究的数据进行荟萃分析,发现胆固醇和脂质通路基因对AMD发病率和进展的影响存在显著异质性。校正多重比较后,我们在荟萃分析中未发现任何胆固醇指标、他汀类药物使用或血脂基因与AMD结局之间存在统计学显著相关性。在一项荟萃分析中,胆固醇指标、他汀类药物使用史或脂质通路基因与AMD的发病率和进展无关。这些发现增加了我们的研究和其他研究的早期报告中的不一致性,这些报告显示高密度脂蛋白胆固醇和总胆固醇与AMD之间存在弱相关性、无相关性或负相关性。
To describe associations of serum lipid levels and lipid pathway genes to the incidence of age-related macular degeneration (AMD). Meta-analysis. Three population-based cohorts. 6950 participants from the Beaver Dam Eye Study (BDES), Blue Mountains Eye Study (BMES) and Rotterdam Study (RS). Participants were followed over 20 years and examined at 5-year intervals. Hazard ratios (HRs) associated with lipid levels per standard deviation above the mean or associated with each additional risk allele for each lipid pathway gene were calculated using random-effects inverse-weighted meta-analysis models, adjusting for known AMD risk factors. Incidence of AMD. The average 5-year incidences of early AMD were 8.1%, 15.1%, and 13.0% in the BDES, BMES, and RS, respectively. Substantial heterogeneity in the effect of cholesterol and lipid pathway genes on the incidence and progression of AMD was evident when the data from the three studies were combined in meta-analysis. After correction for multiple comparisons, we did not find a statistically significant association between any of the cholesterol measures, statin use, or serum lipid genes and any of the AMD outcomes in the meta-analysis. In a meta-analysis, there were no associations of cholesterol measures, history of statin use, or lipid pathway genes to the incidence and progression of AMD. These findings add to inconsistencies in earlier reports from our studies and others showing weak associations, no associations, or inverse associations of high-density lipoprotein cholesterol and total cholesterol with AMD.
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