Meta-analysis of brain metabolite differences in HIV infection.

Meta-analysis of brain metabolite differences in HIV infection.
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DOI:
10.1016/j.nicl.2020.102436
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发表时间:
2020
期刊:
NeuroImage. Clinical
影响因子:
--
通讯作者:
Zeffiro TA
Zeffiro TA
中科院分区:
其他
文献类型:
--
作者:
Chelala L;O'Connor EE;Barker PB;Zeffiro TA

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Meta-analysis identifies reliable MRS changes associated with chronic HIV infection. BG showed consistently higher tCho/tCr and mI/tCr ratios in HIV infection. Cortical GM and WM showed lower tNAA/tCr, higher tCho/tCr and mI/tCr ratios in HIV. Serostatus effects on GM tNAA/tCr and WM tNAA/tCr declined with calendar year. Higher WM tCho/tCr and mI/tCr may reflect reactive gliosis or myelin turnover. Numerous studies have used magnetic resonance spectroscopy (MRS) neurometabolite measurements to study HIV infection effects. While many have reported differences in total N-Acetylaspartate (tNAA), myo-Inositol (mI), and total Choline (tCho), there have been no meta-analyses performed to evaluate concordance across studies. To evaluate the consistency of HIV serostatus effects on brain metabolites. The sample included studies conducted between 1993 and 2019 reporting HIV infection effects measured using proton MRS. tNAA/tCr ratios (21 papers), tCho/tCr ratios (21 papers), mI/tCr ratios (17 papers) and quantitative tCr (9 papers), sampling from basal ganglia (BG), gray matter (GM), and white matter (WM) were included. Random effects meta-analysis using inverse variance weighting and bias corrected standardized mean differences (SMDs) was used. Meta-regression examined effects of publication year and data acquisition technique differences. BG SMDs related to positive serostatus were −0.10 [−0.39; 0.18] tNAA/tCr, 0.27 [0.05; 0.49] tCho/tCr, 0.60 [0.31; 0.90] mI/tCr, and −0.26 [−0.59; 0.06] tCr. GM SMDs related to serostatus were −0.29 [−0.49; −0.09] tNAA/tCr, 0.37 [0.19; 0.54] tCho/tCr, 0.41 [0.15; 0.68] mI/tCr, and −0.24 [−0.45; −0.03] tCr. WM SMDs related to serostatus were −0.52 [−0.79; −0.25] tNAA/tCr, 0.41 [0.21; 0.61] tCho/tCr, 0.59 [0.24; 0.94] mI/tCr, and −0.03 [−0.25; 0.19] tCr. WM regions showed larger serostatus effect sizes than BG and GM. I2 ranged from 52 to 88% for the metabolite ratios. Both GM and WM tNAA/tCr SMDs were lower with increasing calendar year. Many studies pooled participants with varying treatment, infection, and comorbidity durations. HIV neurometabolite studies showed consistently lower tNAA/tCr, higher tCho/tCr and higher mI/tCr ratios associated with chronic HIV infection. Substantial between-study variation may have resulted from measurement technique variations, study population differences and HIV treatment changes over time. Higher WM tCho/tCr and mI/tCr may reflect reactive gliosis or myelin turnover. Neurometabolite measurements can reliably detect chronic HIV infection effects and may be useful in understanding the pathophysiology of cognitive and sensorimotor decline following HIV infection. This study provides Class II evidence of neurometabolite differences in chronic HIV infection.
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