Infectious Diseases Unit, Hospital Clínic-Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, C/Villarroel 170, 08036 Barcelona, Spain.
AIDS. 2010 Jan 28;24(3):F1-9. doi: 10.1097/QAD.0b013e32833562c5.
To assess the effects of initiating abacavir-containing therapy on plasma lipids and cardiovascular biomarkers.
Sub-study of the BICOMBO study in which participants were randomized to switch their nucleoside backbone to either abacavir/lamivudine or tenofovir/emtricitabine.
We assessed 48-week changes in fasting lipids and several biomarkers including serum high-sensitivity C-reactive protein (hsCRP), monocyte chemoattractant protein-1 (MCP-1), osteoprotegerin, interleukin (IL)-6, IL-10, tumor necrosis factor alpha (TNF-alpha), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), selectin E and P, adiponectin, insulin, and D-dimer in otherwise healthy, virologically suppressed HIV-infected patients randomly switched to abacavir/lamivudine or tenofovir/emtricitabine with no history of cardiovascular disease, no prior abacavir or tenofovir use, and no virological failure or AIDS during follow-up.
Eighty (46 abacavir/lamivudine and 34 tenofovir/emtricitabine) patients were included. Baseline characteristics were similar between groups and between patients in the sub-study vs. those not. There were no significant differences in baseline lipids and markers between groups. Although total (6.5 vs. -6.7%, P < 0.0001) and low-density lipoprotein (LDL) (8.6 vs. -9.1%, P = 0.004) cholesterol increased significantly in the abacavir/lamivudine group relative to the tenofovir/emtricitabine group, we found no significant changes in the biomarkers: CRP (-3.9 vs. 0.0%), MCP-1 (5.9 vs. 4.0%), osteoprotegerin (5.1 vs. -2.8%), IL-6 (0.0 vs. 0.0%), IL-10 (0.0 vs. 0.0%), TNF-alpha (0.0 vs. 0.0%), ICAM-1 (6.6 vs. 5.2%), VCAM-1 (0.02 vs. -0.01%), selectin E (-0.4 vs. 7.8%), selectin P (4.6 vs. 12.6%), insulin (-2.5 vs. 8.8%), adiponectin (-2.2 vs. 15.4%), and D-dimer (0.0 vs. 0.0%) (P > or = 0.12 for all comparisons).
Abacavir/lamivudine increased total and LDL cholesterol compared with tenofovir/emtricitabine, but it did not cause inflammation, endothelial dysfunction, insulin resistance, or hypercoagulability in virologically suppressed HIV-infected patients.
评估起始使用含阿巴卡韦疗法对血浆脂质和心血管生物标志物的影响。
BICOMBO 研究的亚组研究，参与者被随机分配至核苷类逆转录酶抑制剂转换方案组，分别为阿巴卡韦/拉米夫定或替诺福韦/恩曲他滨。
我们评估了 48 周时空腹血脂和几种生物标志物的变化，包括血清高敏 C 反应蛋白（hsCRP）、单核细胞趋化蛋白-1（MCP-1）、骨保护素、白细胞介素（IL）-6、IL-10、肿瘤坏死因子 alpha（TNF-alpha）、细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）、选择素 E 和 P、脂联素、胰岛素和 D-二聚体。这些患者为病毒学抑制的 HIV 感染者，无心血管疾病病史，无阿巴卡韦或替诺福韦用药史，随访期间无病毒学失败或 AIDS。
共纳入 80 例患者（46 例阿巴卡韦/拉米夫定，34 例替诺福韦/恩曲他滨）。两组间和亚组中与未纳入亚组的患者间基线特征相似。组间基线脂质和标志物无显著差异。尽管阿巴卡韦/拉米夫定组总胆固醇（6.5% vs. -6.7%，P < 0.0001）和低密度脂蛋白（LDL）胆固醇（8.6% vs. -9.1%，P = 0.004）显著增加，但我们发现生物标志物无显著变化：CRP（-3.9% vs. 0.0%）、MCP-1（5.9% vs. 4.0%）、骨保护素（5.1% vs. -2.8%）、IL-6（0.0% vs. 0.0%）、IL-10（0.0% vs. 0.0%）、TNF-alpha（0.0% vs. 0.0%）、ICAM-1（6.6% vs. 5.2%）、VCAM-1（0.02% vs. -0.01%）、选择素 E（-0.4% vs. 7.8%）、选择素 P（4.6% vs. 12.6%）、胰岛素（-2.5% vs. 8.8%）、脂联素（-2.2% vs. 15.4%）和 D-二聚体（0.0% vs. 0.0%）（所有比较 P ≥ 0.12）。
与替诺福韦/恩曲他滨相比，阿巴卡韦/拉米夫定增加了总胆固醇和 LDL 胆固醇，但并未在病毒学抑制的 HIV 感染者中引起炎症、内皮功能障碍、胰岛素抵抗或高凝状态。
