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CD4 at HAART Initiation Predicts Long Term CD4 Responses and Mortality from AIDS and non-AIDS Causes in the HIV Outpatient Study (HOPS)
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Reported by jules Levin
17th CROI Feb 16-19 2010 SF
FJ Palella Jr1 , C Armon2, K Buchacz3, B Yangco4, JS Chmiel1, R Novak5, K Wood2, M Durham3, JT Brooks3and the HOPS Investigators
1Northwestern University Feinberg School of Medicine, Chicago, IL; 2Cerner Corporation, Vienna, VA; 3Centers for Disease Control and Prevention (CDC); 4Infectious Disease Research Institute, Tampa, FL;
5University of Illinois College of Medicine at Chicago
CONCLUSIONS:
Lower BL CD4 at HAART initiation was associated with:
· Lower subsequent peak CD4 achieved while on HAART
· Lower CD4 near time of death
· Increased risk of death from AIDS-related and non-AIDS-related causes.
Among persons starting HAART with BL CD4 ≥ 200 and CD4 ≥ 350, deaths with non-AIDS causes comprised the majority of deaths.
RESULTS
Among 1,378 patients median follow-up was 4.2 years and there were 82 deaths.
By baseline (BL) CD4 strata (< 50, 50-199, 200-349, ≥ 350):
· Median peak CD4 achieved after BL was progressively higher at each higher BL CD4 stratum: 392, 443, 644, and 956, p<0.001 for trend (Table 3);
· Crude mortality rates per 100 person-years decreased: 2.80, 1.52, 0.60, and 0.53, p<0.001 for trend;
ABSTRACT
Background: Initiating HAART at higher CD4 cell counts/mm3(CD4) has been demonstrated to result in decreased mortality. We sought to assess the impact of earlier (versus later) HAART initiation upon causes of death, CD4 trajectories after HAART initiation, and CD4 at time of death.
Methods: We studied patients with >6 months (mos) of follow-up (f/u) after starting HAART seen at 10 U.S. clinics during 1996-2007. We analyzed CD4 trajectories (compared using the Jonckheere-Terpstra test) and mortality rate (MR) trends by CD4 at time of HAART start (baseline, BL). We assessed factors associated with mortality using Cox proportional hazards models.
Results: Among 1,378 patients with a CD4 recorded at HAART initiation, median f/u was 4.2 years and 82 died within 6 mos of last contact.
By baseline CD4 strata (< 50, 50-199, 200-349, ≥ 350), we found:
i) median peak CD4 achieved after BL was progressively higher at each higher BL CD4 stratum: 392, 443, 644, and 956, p<0.001 for trend;
ii) the proportions of surviving patients with CD4 ≥350 at 4 years increased: 46%, 59%, 79%, and 95%, p<0.001 for trend;
iii) crude MRs per 100 person-years decreased: 2.80, 1.52, 0.60, and 0.53, p<0.001 for trend; and
iv) among deaths, higher BL CD4 was associated with higher CD4 near death: 68, 186, 245, and 516, p<0.001 for trend.
In multivariable analyses, factors independently associated with mortality were CD4 < 50 (hazard ratio [HR] = 4.6, 95% CI 2.7-7.9) and CD4 50-199 (HR=2.6, 95% CI 1.5-4.8) compared with CD4 ≥ 200, and public insurance (HR=1.73, 95% CI 1.1-2.7).
For persons with known primary cause(s) of death (n= 69), crude mortality rates for patients with AIDS-related (n=33) and non-AIDS-related causes (n=36) decreased with increasing BL CD4 (p<0.001 and p=0.005, respectively, for trend); in the two higher BL CD4 strata (200-349 and ≥ 350) deaths from non-AIDS-related causes predominated (13/17 or 76%).
Median CD4 near death was 27 for patients with AIDS-related causes and 193 for non-AIDS-related causes (p<0.001).
Median CD4 nadir-to-peak increases were greater among persons who survived than among persons who died in the BL CD4 < 50 (401 vs 135, p<0.001; median f/u=57 mos) and BL CD4 50-199 (351 vs 158, p<0.001, median f/u=52 mos) strata, but not in the two higher BL CD4 strata.
Conclusions: Lower BL CD4 at HAART start was associated with lower peak CD4 achieved while on HAART, lower CD4 at time of death, and increased risk of death from AIDS-related and non-AIDS-related causes. Among persons starting HAART with BL CD4 200-349 and ≥ 350, deaths with non-AIDS causes comprised the majority of deaths.
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