Covertly active and progressing neurochemical abnormalities in suppressed HIV infection
Covertly active and progressing neurochemical abnormalities in suppressed HIV infection
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DOI：
10.1212/nxi.0000000000000430
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发表时间：
2018-01-01
影响因子：
8.8
通讯作者：
Rae, Caroline
中科院分区：
文献类型：
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作者：
Cysique, Lucette A.;Juge, Lauriane;Rae, Caroline
目的评估艾滋病毒相关的脑损伤是否是进行性的人与抑制HIV infection.MethodsSeventy-three HIV+病毒抑制的男子和35 HIV-男子，精神和酒精/药物使用障碍筛选，进行神经心理学评估和质子磁共振波谱（H-1-MRS）在基线和23 +/- 5个月后。H-1-MRS包括已知易受HIV和衰老影响的脑区：额叶白色物质（FWM）、后扣带皮层（PCC）和尾状核区（CA）。参考水信号计算主要脑代谢物，如肌酸（Cr：细胞能量的标志物）、N-乙酰天冬氨酸（NAA：神经元完整性的标志物）、胆碱（细胞膜更新的标志物）、谷氨酸/谷氨酰胺（兴奋性/抑制性神经递质）和肌醇（mI：神经炎症的标志物）。神经认知功能下降的实践效果和基线HIV相关的神经认知障碍（HAND）status.ResultsAcross研究期间，44%有完整的认知，42%稳定的手（包括单一的情况下，改善），10%进步的手，和4%事件的手。当根据神经认知轨迹分析神经化学数据时，我们发现与对照组相比，所有亚组的PCC Cr均降低（p < 0.002）。此外，相对于HIV组，稳定的HAND显示FWM Cr下降，发病的HAND显示FWM Cr急剧下降，而进展的HAND的PCC NAA急剧下降，CA NAA下降但稳定。当在组水平（HIV+组与HIV-组）分析神经化学数据时，我们发现在研究期间稳定的异常代谢物浓度：FWM和PCC Cr降低（均p < 0.001），PCC NAA和CA NAA降低（均p < 0.05），PCC mI增加（p < 0.05）。HIV持续时间和历史的手有适度的影响代谢产物的changes.ConclusionsOur研究揭示了隐蔽的活动或进展HIV相关的脑损伤在大多数这个病毒抑制队列，反映了正在进行的神经病理过程，只有部分恶化的历史手和HIV持续时间。长期研究对于确定这些缓慢发展的神经化学异常的预后将是重要的。
ObjectiveTo assess whether HIV-related brain injury is progressive in persons with suppressed HIV infection.MethodsSeventy-three HIV+ virally suppressed men and 35 HIV-men, screened for psychiatric and alcohol/drug use disorders, underwent neuropsychological evaluation and proton magnetic resonance spectroscopy (H-1-MRS) at baseline and after and 23 +/- 5 months. H-1-MRS included brain regions known to be vulnerable to HIV and aging: frontal white matter (FWM), posterior cingulate cortex (PCC), and caudate area (CA). Major brain metabolites such as creatine (Cr: marker of cellular energy), N-acetyl aspartate (NAA: marker of neuronal integrity), choline (marker of cellular membrane turnover), glutamate/glutamine (excitatory/inhibitory neurotransmitter), and myo-Inositol (mI: marker of neuroinflammation) were calculated with reference to water signal. Neurocognitive decline was corrected for practice effect and baseline HIV-associated neurocognitive disorder (HAND) status.ResultsAcross the study period, 44% had intact cognition, 42% stable HAND (including the single case that improved), 10% progressing HAND, and 4% incident HAND. When analyzing the neurochemical data per neurocognitive trajectories, we found decreasing PCC Cr in all subgroups compared with controls (p < 0.002). In addition, relative to the HIV-group, stable HAND showed decreasing FWM Cr, incident HAND showed steep FWM Cr reduction, whereas progressing HAND had a sharply decreasing PCC NAA and reduced but stable CA NAA. When analyzing the neurochemical data at the group level (HIV+ vs HIV-groups), we found stable abnormal metabolite concentrations over the study period: decreased FWM and PCC Cr (both p < 0.001), decreased PCC NAA and CA NAA (both p < 0.05) and PCC mI increase (p < 0.05). HIV duration and historical HAND had modest effects on metabolite changes.ConclusionsOur study reveals covertly active or progressing HIV-related brain injury in the majority of this virally suppressed cohort, reflecting ongoing neuropathogenic processes that are only partially worsened by historical HAND and HIV duration. Longer-term studies will be important for determining the prognosis of these slowly evolving neurochemical abnormalities.