Absolute Count and Percentage of CD4+ Lymphocytes Are Independent Predictors of Disease Progression in HIV‐Infected Persons Initiating Highly Active Antiretroviral Therapy
1Department of Medicine, Division of Infectious Diseases, 2Center for Health Services Research, and 3Department of Biostatistics, Vanderbilt University School of Medicine, and 4Comprehensive Care Center, Nashville, Tennessee; 5EpiQuest Sciences, Inc., Durham, North Carolina, and 6Durham, North Carolina
Background.
Highly active antiretroviral therapy (HAART) is recommended when the absolute CD4+ T lymphocyte count is <200 cells/mm3, and it should be considered when that count is 
200, although the optimal timing when it is 200 is unclear. Because preliminary data had suggested that a low CD4+ T lymphocyte percentage (%CD4) is associated with disease progression in persons initiating HAART who have a higher absolute CD4, we sought to further characterize the predictive utility of %CD4.
Methods.We conducted an observational study of persons in Collaborations in HIV Outcomes Research/US cohort who initiated their first HAART regimen between 1997 and 2004, received 30 days of therapy, and had baseline values of absolute CD4, %CD4, and HIV‐1 RNA. Cox proportional‐hazards models determined associations between %CD4 and disease progression (to either a new AIDS‐defining event [ADE] or death).
Results.Of 1891 persons, 11% were female and 18% were African American; the median age was 38 years. Median follow‐up was 55 months (interquartile range, 23–83 months), and 468 (25%) had disease progression. Multivariable analysis including age, race, sex, HIV‐1 RNA, prior antiretroviral therapy, probable route of infection, prior ADE, absolute CD4, and %CD4 was performed; prior ART (
), injection‐drug use (
), lower absolute CD4 (
), and lower %CD4 (
) predicted disease progression.
Conclusions.%CD4 at initiation of the first HAART regimen predicted disease progression independent of absolute CD4; %CD4 may be used to determine the timing of HAART.
Received 2 June 2006; accepted 15 September 2006; electronically published 21 December 2006.
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Potential conflicts of interest: S.P.R. serves on the CHORUS advisory board; J.S.F. and R.B. were employees of GlaxoSmithKline (GSK) at the time the study was performed. Neither the funding agencies nor GSK were involved in study design, data analysis or interpretation, or drafting of the manuscript.
Financial support: National Institutes of Health (NIH; grant K23 AT002508‐01 to T.H. and grant K24 AI065298 to T.R.S.); Vanderbilt‐Meharry Center for AIDS Research (NIH program P30 AI 54999).