Koethe John R, Grome Heather, Jenkins Cathy A, Kalams Spyros A, Sterling Timothy R
aDivision of Infectious DiseasesbDepartment of MedicinecDepartment of BiostatisticsdDepartment of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
AIDS. 2016 Jan 2;30(1):83-91. doi: 10.1097/QAD.0000000000000893.
This study assessed the effect of obesity on metabolic and cardiovascular disease risk factors in HIV-infected adults on antiretroviral therapy with sustained virologic suppression.
Observational, comparative cohort study with three group-matched arms: 35 nonobese and 35 obese HIV-infected persons on efavirenz, tenofovir and emtricitabine with plasma HIV-1 RNA less than 50 copies/ml for more than 2 years, and 30 obese HIV-uninfected controls. Patients did not have diabetes or known cardiovascular disease.
We compared glucose tolerance, serum lipids, brachial artery flow-mediated dilation, carotid intima-media thickness, and soluble inflammatory and vascular adhesion markers between nonobese and obese HIV-infected patients, and between obese HIV-infected and HIV-uninfected patients, using Wilcoxon rank-sum tests and multivariate linear regression.
The cohort was 52% men and 48% nonwhite. Nonobese and obese HIV-infected patients did not differ by clinical or demographic characteristics. Obese HIV-uninfected controls were younger than obese HIV-infected patients and less likely to smoke (P < 0.03 for both). Among HIV-infected patients, obesity was associated with greater insulin release, lower insulin sensitivity, and higher serum high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 1 levels (P < 0.001), but similar lipid profiles, sCD14, sCD163, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1, and carotid intima-media thickness and flow mediated dilation. In contrast, Obese HIV-infected patients had adverse lipid changes, and greater circulating intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and sCD14, compared with obese HIV-uninfected controls after adjusting for age and other factors.
Obesity impairs glucose metabolism and contributes to circulating high-sensitivity C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 1 levels, but has few additive effects on dyslipidemia and endothelial activation, in Obese HIV-infected adults on long-term antiretroviral therapy.
本研究评估了肥胖对接受抗逆转录病毒治疗且病毒学得到持续抑制的HIV感染成人的代谢和心血管疾病危险因素的影响。
观察性、比较队列研究，设有三个组匹配臂：35名非肥胖和35名肥胖的HIV感染者，接受依非韦伦、替诺福韦和恩曲他滨治疗，血浆HIV-1 RNA低于50拷贝/毫升超过2年，以及30名肥胖的未感染HIV的对照者。患者无糖尿病或已知心血管疾病。
我们使用Wilcoxon秩和检验和多变量线性回归，比较了非肥胖和肥胖HIV感染患者之间，以及肥胖HIV感染和未感染HIV患者之间的葡萄糖耐量、血脂、肱动脉血流介导的扩张、颈动脉内膜中层厚度，以及可溶性炎症和血管粘附标志物。
该队列中男性占52%，非白人占48%。非肥胖和肥胖HIV感染患者在临床或人口统计学特征上无差异。肥胖的未感染HIV的对照者比肥胖的HIV感染患者年轻，吸烟可能性更小（两者P均<0.03）。在HIV感染患者中，肥胖与更高的胰岛素释放、更低的胰岛素敏感性以及更高的血清高敏C反应蛋白、白细胞介素-6和肿瘤坏死因子-α受体1水平相关（P<0.001），但血脂谱、可溶性CD14、可溶性CD163、细胞间粘附分子1和血管细胞粘附分子1、颈动脉内膜中层厚度和血流介导的扩张相似。相比之下，在调整年龄和其他因素后，肥胖的HIV感染患者与肥胖的未感染HIV的对照者相比，有不良的血脂变化，以及更高的循环细胞间粘附分子1、血管细胞粘附分子1和可溶性CD14。
在接受长期抗逆转录病毒治疗的肥胖HIV感染成人中，肥胖损害葡萄糖代谢，并导致循环中的高敏C反应蛋白、白细胞介素-6和肿瘤坏死因子-α受体1水平升高，但对血脂异常和内皮激活几乎没有叠加影响。
