To assess whether nonelevated cerebrospinal fluid (CSF) markers could delineate inactive AIDS dementia complex (ADC) in patients receiving highly active antiretroviral therapy (HAART), using neuropsychologic performance change as an indicator of ADC stability.
We used data from the abacavir (ABC) ADC trial (n = 78) and examined the patients' neuropsychologic performance change with the Reliable Change Index according to 3 cutoff groups: (1) CSF viral load (VL) <100 copies/mL, (2) CSF β-2 microglobulin (β2m) <2.2 mg/L, and (3) CSF VL and CSF β2m below cutoffs.
CSF marker cutoff groups did not define neuropsychologic change. Linear regression showed that only CSF VL was a weak predictor of neuropsychologic performance change.
HAART-treated ADC patients with baseline CSF markers of viral and immunologic inactivity did not necessarily have inactive ADC when followed over 12 weeks. More sensitive CSF markers to judge the activity of ADC are urgently needed, whereas the interpretation of these markers should be considered with caution in HAART-treated ADC patients.
From *St. Vincent's Hospital Clinical School, University of New South Wales, and St. Vincent's Hospital, Darlinghurst, Sydney, Australia; †Department of Neurology and Centre for Immunology, National Centre in HIV Epidemiology and Clinical Research, St. Vincent's Hospital, Darlinghurst, Sydney, Australia; ‡St. Michael's Hospital, Toronto, Ontario, Canada; §Psychological Medicine Unit, South Kensington and Chelsea Mental Health Centre, Imperial College, London, United Kingdom; ∥HIV Neuroscience Group, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD; ¶Department of Neurology, San Francisco General Hospital, San Francisco, CA; #Private practice, West Hollywood, CA; **HIV Neurobehavioral Research Center, San Diego, CA; ††Department of Neurology, Washington University Medical Center, St. Louis, MO; ‡‡Department of Neurophysiology, Mt. Sinai Medical Center, New York, NY; §§St. Vincent's Hospital, New York, NY; ∥∥Department of Neurology, University of North Carolina School of Medicine, Chapel Hill, NC; ¶¶Section of Neurology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; ##Sergievsky Center, Columbia University of Physicians and Surgeons, New York, NY; and ***GlaxoWellcome, Inc., Research Triangle Park, NC.
Received for publication September 10, 2004; accepted April 1, 2005.
Supported by GlaxoSmithKline and grants NS44807 N26643 and NS49807 from the National Institutes of Health, USA.
Reprints: Lucette Cysique, Immunology B, Infectious Diseases Department, Xavier Building, Level 4, St. Vincent's Hospital, Darlinghurst, Sydney 2010, New South Wales, Australia (e-mail: email@example.com).