QUINOLINIC ACID IN THE CEREBROSPINAL-FLUID OF CHILDREN WITH SYMPTOMATIC HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DISEASE - RELATIONSHIPS TO CLINICAL STATUS AND THERAPEUTIC RESPONSE

Quinolinic acid (QUIN) is a neurotoxin implicated in the neurologic de ficits associated with human immunodeficiency virus type 1 (HIV-1) inf ection. Forty children with symptomatic HIV-1 disease had elevated (P < .001) cerebrospinal fluid (CSF) QUIN levels (55.8 +/- 8.9 nM) compar ed with controls (14.9 +/- 3.0 nM). Age-adjusted CSF QUIN concentratio ns in HIV-1-infected children were predicted by the general index of m ental 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 patie nts had higher CSF QUIN levels than patients without encephalopathy (7 9.6 +/- 16.1 vs. 32.7 +/- 6.7 nM, P < .01). CSF QUIN concentrations we re also higher (P < .001) in patients who died less-than-or-equal-to 3 years after their baseline assessment, compared with those who were s till alive. These results warrant further investigation of CSF QUIN in HIV-infected children as a mediator of neurologic dysfunction and a s upplemental marker of neurologic disease, particularly when combined w ith measures of neurocognitive functioning.