艾滋病毒感染者的载脂蛋白 e 基因多态性与血浆血脂:一项横断面研究。

M A Kuti, O T Bamidele, N S Nduka, O Olaniyi, O A Ogundeji, K S Adedapo, O A Awolude
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引用次数: 0

摘要

背景和目的:动脉粥样硬化性心血管疾病的一个主要可改变风险因素是脂质和脂蛋白代谢异常,这在艾滋病及其治疗中经常出现。载脂蛋白 E 是一种在血浆脂质平衡中起重要作用的蛋白质,其基因等位基因已被证明会导致血脂异常。我们研究了载脂蛋白-E基因多态性对接受蛋白酶抑制剂治疗的艾滋病毒感染者血浆脂质水平的影响:这是一项针对成年 HIV 感染者的横断面研究。测量空腹血浆中的血脂、载脂蛋白-B 和载脂蛋白-A。使用 Seeplex Apo-E ACE 基因分型试剂盒对载脂蛋白-E 基因型进行扩增和分析。用非参数分析方法比较了定量值的差异:研究共招募了 84 人,其中 75% 的人受到病毒抑制。3种同源基因型的低密度脂蛋白胆固醇(LDL-C)、载脂蛋白B(Apo-B)和载脂蛋白A1(Apo-A1)水平有显著差异。与载脂蛋白ε3/ε3患者相比,载脂蛋白ε2/ε2患者的低密度脂蛋白胆固醇更高(3.26 (3.61) mmol/L vs. 2.76 (1.28) mmol/L,p = 0.010)。载脂蛋白ε4/ε4患者的载脂蛋白-A1低于载脂蛋白ε3/ε3患者(0.84 (0.48) g/dL vs. 1.27 (0.70) g/dL,p =0.009)。与同组相比,杂合基因型的载脂蛋白ε2/ε3甘油三酯水平较低:1.33 (0.65) mmol/ L vs. 1.86 (1.11) mmol/L,p = 0.045:载脂蛋白 E 基因的多态性可能对接受 PI 治疗的 PLHIV 患者的血浆脂质和载脂蛋白水平有显著影响。这可能会对心血管疾病风险评估产生影响。
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APOLIPOPROTEIN E GENE POLYMORPHISMS AND PLASMA LIPIDS IN PERSONS LIVING WITH HIV: A CROSS SECTIONAL STUDY.

Background and objective: A major modifiable risk factor for atherosclerotic cardiovascular disease is abnormalities in lipid and lipoprotein metabolism which are frequently seen in HIV as well as its treatment. Apo-E is a protein that is important in plasma lipid homeostasis and its genetic alleles have been shown to contribute to lipid abnormalities. We examined for the effect of Apo-E gene polymorphisms on plasma lipid levels in PLHIV on protease inhibitor therapy.

Methods: This was a cross-sectional study conducted among adult persons living with HIV. Lipid profile, Apo-B and Apo-A were measured in fasting plasma. Amplification and analysis of Apo-E genotypes were determined using the Seeplex Apo-E ACE genotyping kit. Differences in quantitative values were compared with non-parametric analysis methods.

Results: Eighty-four persons were recruited into the study, 75% of whom were virally suppressed. The 3 homozygous genotypes had significantly different levels of low-density lipoprotein cholesterol (LDL-C), Apolipoprotein B (Apo-B) and Apolipoprotein A1 (Apo-A1). Persons with apo ε2/ε2 had higher LDL-C compared to those with apo ε3/ε3 (3.26 (3.61) mmol/L vs. 2.76 (1.28) mmol/L, p = 0.010). Those with apo ε4/ε4 had lower Apo-A1 compared to those with apo ε3/ε3 (0.84 (0.48) g/dL vs. 1.27 (0.70) g/dL, p =0.009). Compared with the same group, the heterozygous genotype, apo ε2/ε3 had lower triglyceride levels :1.33 (0.65) mmol/ L vs. 1.86 (1.11) mmol/L, p = 0.045.

Conclusion: Polymorphisms in the Apo-E gene may have significant influences on plasma lipid and apolipoprotein levels in PLHIV on PI therapy. This may have implications for the assessment of risk for cardiovascular disease.

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