Cortical NAA deficits in HIV infection without dementia: Influence of alcoholism comorbidity
Cortical NAA deficits in HIV infection without dementia: Influence of alcoholism comorbidity
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DOI：
10.1038/sj.npp.1300723
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发表时间：
2005-07-01
影响因子：
7.6
通讯作者：
Sullivan, EV
中科院分区：
文献类型：
--
作者：
Pfefferbaum, A;Adalsteinsson, E;Sullivan, EV
酒精中毒合并症在人类免疫缺陷病毒（HIV）感染者中非常普遍。已知每种情况都会影响大脑结构、功能和新陈代谢，但对大脑的综合影响最近才被考虑。单体素，质子磁共振波谱（MRS）已经产生了敏感的措施，早期大脑恶化的进展，艾滋病毒，但有有限的覆盖范围的新皮层，而MRS成像（MRSI）可以同时询问大区域的皮层。其中包括15名感染艾滋病毒+酗酒的男性、9名仅感染艾滋病毒的男性、8名仅酗酒的男性（戒酒3-17个月）和23名对照。两组HIV感染者的T细胞计数相匹配，并且没有痴呆;两组酗酒者的一生饮酒量相对匹配。我们使用MRSI和可变密度螺旋序列来量化上级顶枕皮质中的主要质子代谢物-N-乙酰天冬氨酸（NAA）、肌酸（Cr）和胆碱（Cho）。代谢产物以绝对单位和NAA/Cr比值表示。NAA和Cr的组效应显著。只有HIV +酒精中毒组受到显著影响，表现出0.8 SD的NAA和1.0 SD的Cr赤字。这些缺陷与高效抗逆转录病毒治疗（HAART）状态无关。无论是艾滋病毒感染还是酒精中毒，都不会单独导致顶枕叶皮质代谢物异常，但每种疾病都有一种倾向，当疾病复合时，都会使受影响的个体面临更高的神经元损害风险。此外，使用的绝对措施显示赤字NAA和铬，如果这些代谢物表示为一个比率，将无法检测到。
Alcoholism comorbidity is highly prevalent in individuals infected with human immunodeficiency virus ( HIV). Each condition is known to affect brain structure, function, and metabolism, but the combined effects on the brain have only recently been considered. Single-voxel, proton MR spectroscopy ( MRS) has yielded sensitive measures of early brain deterioration in the progression of HIV, but has limited coverage of neocortex, whereas MRS imaging ( MRSI) can simultaneously interrogate large regions of cortex. Included were 15 men with HIV + alcoholism, nine men with HIV alone, eight men with alcoholism alone ( abstinent for 3-17 months), and 23 controls. The two HIV groups were matched in T-cell count and were not demented; the two alcoholism groups were relatively matched in lifetime alcohol consumption. We used MRSI with a variable-density spiral sequence to quantify major proton metabolites-N-acetylaspartate ( NAA), creatine ( Cr), and choline ( Cho) Fin the superior parietal-occipital cortex. Metabolites were expressed in absolute units and as the NAA/Cr ratio. Significant group effects were present for NAA and Cr. Only the HIV + alcoholism group was significantly affected, exhibiting a 0.8 SD deficit in NAA and a 1.0 SD deficit in Cr. The deficits were not related to highly active antiretroviral therapy ( HAART) status. Neither HIV infection nor alcoholism independently resulted in parietal-occipital cortical metabolite abnormalities, yet each disease carried a liability that put affected individuals at a heightened risk of neuronal compromise when the diseases were compounded. Further, the use of absolute measures revealed deficits in NAA and Cr that would have gone undetected if these metabolites were expressed as a ratio.