McArthur J C, Nance-Sproson T E, Griffin D E, Hoover D, Selnes O A, Miller E N, Margolick J B, Cohen B A, Farzadegan H, Saah A
Johns Hopkins Medical Institutions, Baltimore, MD.
Neurology. 1992 Sep;42(9):1707-12. doi: 10.1212/wnl.42.9.1707.
We measured serum and CSF beta 2-microglobulin (beta 2M) levels in HIV-1 seropositive individuals with and without dementia to determine the frequency and diagnostic utility of elevation of CSF beta 2M. We compared 34 samples from 27 patients with HIV-1 dementia with 110 samples from 54 HIV-1 seropositive participants in the Multicenter AIDS Cohort Study, none of whom had progressive dementia. Neurosyphilis and CNS opportunistic processes were excluded in all subjects. We stratified the nondemented subjects by duration of HIV seropositivity and peripheral blood CD4 count. Compared with the nondemented group, demented subjects had significantly higher CSF total protein, IgG%, and CSF albumin/serum albumin ratios. A highly significant association was found between elevated CSF beta 2M and reduced CD4 count (p less than 0.0001). No significant differences were noted between the demented and nondemented groups in CSF WBC count or in the frequency of CSF HIV-1 isolation. The mean CSF beta 2M was 1.9 mg/l in the nondemented subjects compared with 4.2 mg/l in those with dementia (p less than 0.0001). We derived a cutoff of 3.8 mg/l from the distribution of CSF beta 2M in the nondemented group. The determination of CSF beta 2M had a sensitivity of 44%, specificity of 90%, and a positive predictive value of 88% for diagnosis of HIV dementia when compared with nondemented subjects with CD4 counts less than 200. In those without dementia, there was a strong correlation between serum and CSF beta 2M (r = 0.50, p less than 0.0001), but in demented subjects CSF beta 2M was elevated independently of serum levels, suggesting that CSF beta 2M is produced within the brain in HIV dementia. In the absence of CNS opportunistic processes, elevated CSF beta 2M greater than 3.8 mg/l is a clinically useful marker for HIV dementia.
我们检测了患有和未患痴呆症的HIV-1血清反应阳性个体的血清和脑脊液β2-微球蛋白（β2M）水平，以确定脑脊液β2M升高的频率及其诊断效用。我们将27例患有HIV-1痴呆症患者的34份样本与多中心艾滋病队列研究中54例HIV-1血清反应阳性参与者的110份样本进行了比较，这些参与者均无进行性痴呆。所有受试者均排除了神经梅毒和中枢神经系统机会性病变。我们根据HIV血清反应阳性持续时间和外周血CD4计数对未患痴呆症的受试者进行了分层。与未患痴呆症的组相比，患痴呆症的受试者脑脊液总蛋白、IgG%以及脑脊液白蛋白/血清白蛋白比值显著更高。脑脊液β2M升高与CD4计数降低之间存在高度显著的关联（p<0.0001）。在脑脊液白细胞计数或脑脊液HIV-1分离频率方面，患痴呆症组与未患痴呆症组之间未发现显著差异。未患痴呆症的受试者脑脊液β2M平均为1.9mg/L，而患痴呆症的受试者为4.2mg/L（p<0.0001）。我们从未患痴呆症组脑脊液β2M的分布得出临界值为3.8mg/L。与CD4计数低于200的未患痴呆症受试者相比，脑脊液β2M检测对HIV痴呆症诊断的敏感性为44%，特异性为90%，阳性预测值为88%。在未患痴呆症的受试者中，血清和脑脊液β2M之间存在强相关性（r = 0.50，p<0.0001），但在患痴呆症的受试者中，脑脊液β2M独立于血清水平升高，这表明在HIV痴呆症中脑脊液β2M是在脑内产生的。在无中枢神经系统机会性病变的情况下，脑脊液β2M大于3.8mg/L升高是HIV痴呆症的一个临床有用标志物。
