Quinolinic Acid in the Cerebrospinal Fluid of Children with Symptomatic Human Immunodeficiency Virus Type 1 Disease: Relationships to Clinical Status and Therapeutic Response

• Published in: The Journal of infectious diseases 1993-12, Vol.168 (6), p.1380-1386
• Main Authors: Brouwers, Pim, Heyes, Melvyn P., Moss, Howard A., Wolters, Pam L., Poplack, David G., Markey, Sanford P., Pizzo, Philip A.
• Format: Article
• Language: English
• Subjects: Acquired Immunodeficiency Syndrome - cerebrospinal fluid; Acquired Immunodeficiency Syndrome - drug therapy; Acquired Immunodeficiency Syndrome - mortality; Acquired Immunodeficiency Syndrome - physiopathology; AIDS; AIDS Dementia Complex - cerebrospinal fluid; Analysis of Variance; Biological and medical sciences; Brain; Central nervous system; Cerebrospinal fluid; Child; Child health services; Child, Preschool; Cognition; Encephalopathies; Female; HIV 1; human immunodeficiency virus 1; Humans; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Infant; Infections; Major Articles; Male; Medical sciences; Nervous system diseases; Pediatrics; Quinolinic Acid - cerebrospinal fluid; Zidovudine - therapeutic use
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/168.6.1380

Quinolinic acid (QUIN) is a neurotoxin implicated in the neurologic deficits associated with human immunodeficiency virus type 1 (HIV-1) infection. Forty children with symptomatic HIV-1 disease had elevated (P < .001) cerebrospinal fluid (CSF) QUIN levels (55.8 ± 8.9 nM) compared with controls (14.9 ± 3.0 nM). Age-adjusted CSF QUIN concentrations in HIV-1-infected children were predicted by the general index of mental abilities (GIMA, from an age-appropriate intelligence test; r = -0.45, P < .01). Zidovudine therapy reduced CSF QUIN from 64.1 ± 16.3 to 19.7 ± 5.2 nM (P < .01;N = 16) and increased GIMA from 76.8 ± 5.2 to 87.2 ± 6.3 (P < .001). Encephalopathic HIV-1-infected patients had higher CSF QUIN levels than patients without encephalopathy (79.6 ± 16.1 vs. 32.7 ± 6.7 nM, P < .01). CSF QUIN concentrations were also higher (P < .001) in patients who died ⩾3 years after their baseline assessment, compared with those who were still alive. These results warrant further investigation of CSF QUIN in HIV-infected children as a mediator of neurologic dysfunction and a supplemental marker of neurologic disease, particularly when combined with measures of neurocognitive functioning.