Neurometabolite Alterations Associated With Cognitive Performance in Perinatally HIV-Infected Children

被引：22

作者：

Van Dalen, Yvonne W. ^{[1
]}

Blokhuis, Charlotte ^{[1
]}

Cohen, Sophie ^{[1
]}

Ter Stege, Jacqueline A. ^{[1
,2
]}

Teunissen, Charlotte E. ^{[3
,4
]}

Kuhle, Jens ^{[5
]}

Kootstra, Neeltje A. ^{[6
]}

Scherpbier, Henriette J. ^{[1
]}

Kuijpers, Taco W. ^{[1
]}

Reiss, Peter ^{[7
,8
,9
,10
]}

Majoie, Charles B. L. M. ^{[11
,12
]}

Caan, Matthan W. A. ^{[12
]}

Pajkrt, Dasja ^{[1
]}

机构：

[1] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Dept Pediat Hematol Immunol & Infect Dis, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

[2] Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, Psychosocial Dept, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

[3] Vrije Univ Amsterdam, Med Ctr, Dept Clin Chem, Neurochem Lab & Biobank, Amsterdam, Netherlands

[4] Neurocampus Amsterdam, Amsterdam, Netherlands

[5] Univ Basel Hosp, Dept Med, Dept Biomed & Clin Res, Neurol, CH-4031 Basel, Switzerland

[6] Acad Med Ctr, Dept Expt Immunol, Amsterdam, Netherlands

[7] Acad Med Ctr, Dept Global Hlth, Amsterdam, Netherlands

[8] Acad Med Ctr, Amsterdam Inst Global Hlth & Dev, Amsterdam, Netherlands

[9] Univ Amsterdam, Acad Med Ctr, HIV Monitoring Fdn, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

[10] Univ Amsterdam, Acad Med Ctr, Dept Internal Med, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

[11] Univ Amsterdam, Acad Med Ctr, Ctr Infect & Immun Amsterdam, Div Infect Dis, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

[12] Univ Amsterdam, Acad Med Ctr, Dept Radiol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands

来源：

MEDICINE | 2016年 / 95卷 / 12期

基金：

新加坡国家研究基金会; 荷兰研究理事会;

关键词：

MAGNETIC-RESONANCE-SPECTROSCOPY; HUMAN-IMMUNODEFICIENCY-VIRUS; CEREBROSPINAL-FLUID; METABOLITE CONCENTRATIONS; ANTIRETROVIRAL THERAPY; MONOCYTE ACTIVATION; CEREBRAL INJURY; BRAIN; NEURODEGENERATION; ENCEPHALOPATHY;

D O I：

10.1097/MD.0000000000003093

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Despite treatment with combination antiretroviral therapy (cART), cognitive impairment is still observed in perinatally HIV-infected children. We aimed to evaluate potential underlying cerebral injury by comparing neurometabolite levels between perinatally HIV-infected children and healthy controls. This cross-sectional study evaluated neurometabolites, as measured by Magnetic Resonance Spectroscopy (MRS), in perinatally HIV-infected children stable on cART (n = 26) and healthy controls (n = 36). Participants were included from a cohort of perinatally HIV-infected children and healthy controls, matched group-wise for age, gender, ethnicity, and socio-economic status. N-acetylaspartate (NAA), glutamate (Glu), myo-inositol (ml), and choline (Cho) levels were studied as ratios over creatine (Cre). Group differences and associations with HIV-related parameters, cognitive functioning, and neuronal damage markers (neurofilament and total Tau proteins) were determined using age-adjusted linear regression analyses. HIV-infected children had increased Cho:Cre in white matter (HIV-infected = 0.29 +/- 0.03; controls = 0.27 +/- 0.03; P value = 0.045). Lower nadir CD4+ T-cell Z-scores were associated with reduced neuronal integrity markers NAA:Cre and Glu:Cre. A Centers for Disease Control and Prevention (CDC) stage C diagnosis was associated with higher glial markers Cho:Cre and mI:Cre. Poorer cognitive performance was mainly associated with higher Cho:Cre in HIV-infected children, and with lower NAA:Cre and Glu:Cre in healthy controls. There were no associations between neurometabolites and neuronal damage markers in blood or CSF. Compared to controls, perinatally HIV-infected children had increased Cho:Cre in white matter, suggestive of ongoing glial proliferation. Levels of several neurometabolites were associated with cognitive performance, suggesting that MRS may be a useful method to assess cerebral changes potentially linked to cognitive outcomes.

引用

页数：10

共 43 条

[1] CSF neurofilament protein (NFL) -: a marker of active HIV-related neurodegeneration [J].