Prevalence of non-confounded HIV-associated neurocognitive impairment in the context of plasma HIV RNA suppression

Prevalence of non-confounded HIV-associated neurocognitive impairment in the context of plasma HIV RNA suppression
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DOI:
10.1007/s13365-011-0021-x
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发表时间:
2011-04-01
影响因子:
3.2
通讯作者:
Brew, Bruce J.
Brew, Bruce J.
中科院分区:
医学4区
文献类型:
--
作者:
Cysique, Lucette A.;Brew, Bruce J.

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HIV相关的神经认知障碍已知发生在成功的抗逆转录病毒联合治疗(cART;血浆HIV RNA < 50拷贝/ml)的背景下。在这里,我们在没有医学或精神病学混淆的情况下,对其患病率和性质进行了新的分析,否则可能会增加患病率。我们招募了116名接受cART治疗的晚期HIV +个体(51%病毒抑制(VS))。他们被筛查为活动性丙型肝炎,目前的物质使用障碍,并通过标准的神经心理学(NP)测试进行评估。我们的研究结果显示,在整个样本中,VS个体中有18.1%(21/116)发生NP损伤,与发现NP损伤而非VS的24.1%(28/116)无统计学差异。与NP正常VS者相比,VS个体的NP损伤与当前cART持续时间较短和发病前能力较低有关。在np受损的VS个体中,较高的cART CNS穿透效能往往与较低的认知严重程度相关。目前的CD4细胞计数、抑郁症状和过去的中枢神经系统hiv相关疾病并不能明确解释VS个体中持续的NP损伤。总之,尽管抑制了全身病毒载量,但非混杂hiv相关np损害的患病率达到18.1%。在这种持续缺陷的潜在解释中,疾病的“燃尽”形式和免疫重建炎症综合征是不太可能的解释,而较短的当前cART持续时间和较低的发病前智力是重要的。尽管如此,使用后两个因素的预测建模错误分类27%,并且灵敏度低(43%),强调其他尚未定义的因素是有效的。
HIV-associated neurocognitive disorder is known to occur in the context of successful combination antiretroviral therapy (cART; plasma HIV RNA < 50 copies/ml). Here, we newly provide an analysis of its prevalence and nature in the absence of medical or psychiatric confounds that may otherwise inflate the prevalence rate. We enrolled a cohort of 116 advanced HIV + individuals on cART (51% virally suppressed (VS)). They were screened for active Hepatitis C, current substance use disorder and were assessed with standard neuropsychological (NP) testing. Our results showed that out of the entire sample, NP impairment occurred in 18.1% (21/116) in VS individuals which was not statistically different from the 24.1% (28/116) that were found to be NP-impaired and not VS. In comparison with NP-normal-VS persons, NP impairment in VS individuals was associated with shorter duration of current cART and lower pre-morbid ability. Higher cART CNS penetration effectiveness tended to be associated with lesser cognitive severity in NP-impaired VS individuals. Current CD4 cell count, depression symptoms and past CNS HIV-related diseases did not specifically account for persistent NP impairment in VS individuals. In conclusion, despite suppression of systemic viral load, non-confounded HIV-related NP-impairment prevalence reached 18.1%. Of the potential explanations for this persistent deficit, a "burnt-out" form of the disease and immune reconstitution inflammatory syndrome were the less likely explanations, while a shorter current cART duration and lower pre-morbid intellectual capacity were significant. Nonetheless, predictive modelling with these last two factors misclassified 27% and had low sensitivity (43%) emphasising that other yet-to-be-defined factors were operative.