Progressive Brain Atrophy Despite Persistent Viral Suppression in HIV Patients Older Than 60 Years.

J Acquir Immune Defic Syndr

*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.

Published: November 2017

AI Article Synopsis

  • HIV treatments can suppress the virus to undetectable levels, but they may not prevent brain inflammation and injury, especially in older patients.
  • A study compared brain atrophy rates in HIV-infected individuals over 60 years old with healthy aging controls, revealing that those with HIV experience significantly faster brain atrophy in several areas.
  • Even with effective viral suppression, older adults with HIV showed more pronounced brain atrophy than their healthy counterparts, suggesting that factors related to HIV or the aging process may contribute to this accelerated decline.

Article Abstract

Background: 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.

Methods: 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).

Results: 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.

Conclusions: 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5634906PMC
http://dx.doi.org/10.1097/QAI.0000000000001489DOI Listing

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