Clifford Katherine M, Samboju Vishal, Cobigo Yann, Milanini Benedetta, Marx Gabriel A, Hellmuth Joanna M, Rosen Howard J, Kramer Joel H, Allen Isabel E, Valcour Victor G
*Memory and Aging Center, Department of Neurology, University of California San Francisco, San Francisco, CA; †The Robert Larner, M.D. College of Medicine, University of Vermont, Burlington, VT; ‡Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA; and §AIDS Research Institute, University of California at San Francisco, San Francisco, CA.
J Acquir Immune Defic Syndr. 2017 Nov 1;76(3):289-297. doi: 10.1097/QAI.0000000000001489.
Current HIV treatments are successful at suppressing plasma HIV RNA to undetectable levels for most adherent patients. Yet, emerging evidence suggests that viral suppression will inadequately control inflammation and mitigate risk for progressive brain injury. We sought to quantify differences in longitudinal brain atrophy rates among older virally suppressed HIV-infected participants compared with that of healthy aging participants.
We examined longitudinal structural brain magnetic resonance imaging atrophy rates using region of interest assessments and voxel-wise tensor-based morphometry in HIV-infected participants older than 60 years (n = 38) compared with age-matched HIV-uninfected healthy and cognitively normal controls (n = 24).
The mean age of participants was 63 years, the mean estimated duration of infection was 21 years, and the median duration of documented viral suppression was 3.2 years. Average proximal and nadir CD4 counts were 550 and 166, respectively; 15/38 (39%) met criteria for HIV-associated neurocognitive disorder. In models adjusting for age and sex, HIV serostatus was associated with more rapid average annualized rates of atrophy in the cerebellum (0.42% vs. 0.02%, P = 0.016), caudate (0.74% vs. 0.03%, P = 0.012), frontal lobe (0.48% vs. 0.01%, P = 0.034), total cortical gray matter (0.65% vs. 0.16%, P = 0.027), brainstem (0.31% vs. 0.01%, P = 0.026), and pallidum (0.73% vs. 0.39%, P = 0.046). Among those with HIV, atrophy rates did not differ statistically by cognitive status.
Despite persistent control of plasma viremia, these older HIV-infected participants demonstrate more rapid progressive brain atrophy when compared with healthy aging. Either HIV or other factors that differ between older HIV-infected participants and healthy controls could be responsible for these differences.
对于大多数坚持治疗的患者，目前的HIV治疗能够成功地将血浆HIV RNA抑制到检测不到的水平。然而，新出现的证据表明，病毒抑制不足以控制炎症和降低进行性脑损伤的风险。我们试图量化与健康衰老参与者相比，年龄较大、病毒得到抑制的HIV感染者的纵向脑萎缩率差异。
我们使用感兴趣区域评估和基于体素的张量形态测量法，对60岁以上的HIV感染者（n = 38）与年龄匹配的未感染HIV的健康且认知正常的对照者（n = 24）进行纵向脑结构磁共振成像萎缩率检查。
参与者的平均年龄为63岁，平均估计感染持续时间为21年，记录的病毒抑制中位持续时间为3.2年。平均近端和最低点CD4细胞计数分别为550和166；15/38（39%）符合HIV相关神经认知障碍的标准。在调整年龄和性别的模型中，HIV血清学状态与小脑（0.42%对0.02%，P = 0.016）、尾状核（0.74%对0.03%，P = 0.012）、额叶（0.48%对0.01%，P = 0.034）、总皮质灰质（0.65%对0.16%，P = 0.027）、脑干（0.31%对0.01%，P = 0.026）和苍白球（0.73%对0.39%，P = 0.046）的更快的平均年化萎缩率相关。在HIV感染者中，萎缩率在认知状态上没有统计学差异。
尽管血浆病毒血症得到持续控制，但与健康衰老相比，这些年龄较大的HIV感染者表现出更快的进行性脑萎缩。HIV或年龄较大的HIV感染者与健康对照者之间不同的其他因素可能是造成这些差异的原因。
