Asztalos Bela F, Matera Robert, Horvath Katalin V, Horan Michael, Tani Mariko, Polak Joseph F, Skinner Sally, Wanke Christine A
Lipid Metabolism Laboratory, Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA, USA ; Division of Nutrition and Infection, Department of Public Health and Community Medicine, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA, USA.
Lipid Metabolism Laboratory, Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA, USA.
J AIDS Clin Res. 2014 Jun 12;5(7). doi: 10.4172/2155-6113.1000317.
HIV-positive patients have an increased risk for CVD; however, the underlying mechanisms are not well understood. Our goal was to assess traditional and emerging CVD-risk factors in the CARE Study, a well-described cohort of HIV-infected adults.
We analyzed demographic and clinical (viral load, CD4 count, ART regimen, cIMT) data including markers of lipid and glucose homeostasis in 176 HIV-positive subjects receiving regular care for HIV infection.
No significant association between cIMT and LDL-C level was observed. HIV patients had significantly lower level of the large α-1 HDL particles and about 3-fold higher level of the small pre β-1 HDL particles than the normal population, but these parameters were not significantly associated with cIMT. Components of the metabolic syndrome, high TG/low HDL-C, insulin resistance and high BMI, as well as viral load were significant but moderate contributors to increased cIMT.
The major lipid disorder was low HDL-C and high TG level in this HIV-positive cohort. LDL-C was not elevated. These and previously published data indicate that HIV infection and HIV medications influence CVD risk by impairing cholesterol removal (efflux) via ABCA1 from macrophages. Decreasing CVD risk in HIV patients, with impaired cholesterol efflux from macrophages, may require a lower LDL-C goal than recommended for HIV-negative patients and also a better control of TG level.
HIV 阳性患者患心血管疾病(CVD)的风险增加;然而,其潜在机制尚未完全明确。我们的目标是在 CARE 研究中评估传统和新出现的 CVD 风险因素,该研究是一个对感染 HIV 的成年人进行了充分描述的队列。
我们分析了 176 名接受 HIV 感染常规治疗的 HIV 阳性受试者的人口统计学和临床数据(病毒载量、CD4 细胞计数、抗逆转录病毒治疗方案、颈动脉内膜中层厚度[cIMT]),包括脂质和葡萄糖稳态的标志物。
未观察到 cIMT 与低密度脂蛋白胆固醇(LDL-C)水平之间存在显著关联。与正常人群相比,HIV 患者的大α-1高密度脂蛋白(HDL)颗粒水平显著降低,小前β-1 HDL 颗粒水平约高 3 倍,但这些参数与 cIMT 无显著关联。代谢综合征的组成部分,即高甘油三酯/低高密度脂蛋白胆固醇、胰岛素抵抗和高体重指数(BMI),以及病毒载量,是 cIMT 增加的显著但中等程度的促成因素。
在这个 HIV 阳性队列中,主要的脂质紊乱是低 HDL-C 和高甘油三酯水平。LDL-C 未升高。这些以及先前发表的数据表明,HIV 感染和 HIV 药物通过损害巨噬细胞中通过三磷酸腺苷结合盒转运体 A1(ABCA1)的胆固醇清除(流出)来影响 CVD 风险。对于巨噬细胞胆固醇流出受损的 HIV 患者,降低 CVD 风险可能需要比推荐给 HIV 阴性患者更低的 LDL-C 目标,同时更好地控制甘油三酯水平。