Barber T J, Moyle G, Hill A, Jagjit Singh G, Scourfield A, Yapa H M, Waters L, Asboe D, Boffito M, Nelson M
a St Stephen's Centre, Chelsea and Westminster NHS Foundation Trust , London , UK.
b University College London Hospitals NHS Foundation Trust , London , UK.
HIV Clin Trials. 2016 May;17(3):123-30. doi: 10.1080/15284336.2016.1176305.
Ongoing inflammation in controlled HIV infection contributes to non-AIDS comorbidities. High bilirubin appears to exhibit an anti-inflammatory effect in vivo. We therefore examined whether increased bilirubin in persons with HIV was associated with differences in markers of inflammation and cardiovascular, bone, renal disease, and neurocognitive (NC) impairment.
This cross-sectional study examined inflammatory markers in individuals with stable HIV infection treated with two nucleoside reverse transcriptase inhibitors and a boosted protease inhibitor. Individuals recruited were those with a normal bilirubin (NBR; 0-17 μmol/L) or high bilirubin (>2.5 × upper limit of normal). Demographic and anthropological data were recorded. Blood and urine samples were taken for analyses. Pulse wave velocity (PWV) measurement, carotid intimal thickness (CIT), and calcaneal stiffness (CSI) were measured. Males were asked to answer a questionnaire about sexual function; NC testing was performed using CogState.
101 patients were screened, 78 enrolled (43 NBR and 35 HBR). Atazanavir use was significantly higher in HBR. Whilst a trend for lower CIT was seen in those with HBR, no significant differences were seen in PWV, bone markers, calculated cardiovascular risk (Framingham), or erectile dysfunction score. VCAM-1 levels were significantly lower in the HBR group. HBR was associated with lower LDL and triglyceride levels. NBR was associated with a calculated FRAX significantly lower than HBR although no associations were found after adjusting for tenofovir use. No difference in renal markers was observed. Component tests of NC testing revealed differences favouring HBR but overall composite scores were similar.
High bilirubin in the context of boosted PI therapy was found not to be associated with differences in with the markers examined in this study. Some trends were noted and, on the basis of these, a larger, clinical end point study is warranted.
在已控制的HIV感染中，持续的炎症会导致非艾滋病合并症。高胆红素似乎在体内具有抗炎作用。因此，我们研究了HIV感染者胆红素升高是否与炎症、心血管、骨骼、肾脏疾病及神经认知（NC）损害标志物的差异有关。
这项横断面研究检测了接受两种核苷类逆转录酶抑制剂和一种增强型蛋白酶抑制剂治疗的稳定HIV感染者的炎症标志物。招募的个体为胆红素正常（NBR；0 - 17μmol/L）或高胆红素（>2.5×正常上限）者。记录人口统计学和人体测量学数据。采集血液和尿液样本进行分析。测量脉搏波速度（PWV）、颈动脉内膜厚度（CIT）和跟骨硬度（CSI）。男性被要求回答一份关于性功能的问卷；使用CogState进行NC测试。
筛查了101例患者，78例入组（43例NBR和35例HBR）。HBR组使用阿扎那韦的比例显著更高。虽然HBR者的CIT有降低趋势，但在PWV、骨标志物、计算的心血管风险（弗雷明汉）或勃起功能障碍评分方面未发现显著差异。HBR组的血管细胞黏附分子-1（VCAM-1）水平显著更低。HBR与更低的低密度脂蛋白和甘油三酯水平相关。NBR与计算的骨折风险评估工具（FRAX）显著低于HBR相关，尽管在调整替诺福韦使用后未发现相关性。未观察到肾脏标志物有差异。NC测试的分项测试显示有利于HBR的差异，但总体综合评分相似。
发现在增强型蛋白酶抑制剂治疗背景下的高胆红素与本研究中检测的标志物差异无关。注意到了一些趋势，基于这些，有必要开展一项更大规模的临床终点研究。
