Changes in CD4+ cell count and the risk of opportunistic infection or death after highly active antiretroviral treatment. Groupe d'Epidémiologie Clinique du SIDA en Aquitaine.

Abstract

OBJECTIVE:

To study the relationship between the CD4+ cell response after initiation of protease inhibitors and the occurrence of opportunistic infections and survival.

DESIGN:

Prospective observational cohort study.

METHODS:

HIV-1-seropositive subjects followed-up in HIV centres of Bordeaux University Hospital, Southwest France who were prescribed at least one available protease inhibitor between January and December 1996 were included in this analysis. A Cox model estimated the independent effect of baseline covariates and CD4+ cell response, considered as a time-dependent covariate, on the occurrence of new AIDS-defining opportunistic infection, new AIDS-defining events, new AIDS-defining opportunistic infection or death.

RESULTS:

A total of 556 HIV-positive patients were prescribed at least one protease inhibitor: 34% saquinavir, 52% indinavir, and 14% ritonavir. Median CD4+ cell count at baseline was 95 x 10(6)/l and mean plasma HIV RNA was 5.0 log10 copies/ml. After a median follow-up of 230 days, 65 patients experienced a new episode of opportunistic infection, 79 patients experienced at least one AIDS-defining event, and 24 had died. On average, the increase in CD4+ cell count was 42 x 10(6)/l (SD, 74) after a median of 49 days. In the multivariate analysis of opportunistic infection or death, each 50% higher CD4+ cell count at baseline was associated with a 23% reduction [95% confidence interval (CI), 14-30] of risk. Each 50% increase in CD4+ cell count during follow-up was associated with a 9% reduction (95% CI, 2-15) of risk, adjusted for the presence of AIDS prior to protease inhibitor therapy (hazard ratio, 3.76 versus absence of AIDS; P < 0.01) and haemoglobin level (hazard ratio, 0.48 if > 11 g/dl versus <11 g/dl; P < 0.01).

CONCLUSION:

Our results show, at least indirectly, how protease inhibitors might produce clinical stabilization. This result may be due to improved functionality of CD4+ cells in patients started on protease inhibitors.

• Authors: G Chêne, C Binquet, J F Moreau, D Neau, I Pellegrin, D Malvy, J Ceccaldi, D Lacoste, F Dabis
• Journal: AIDS (London, England) (AIDS) Vol. 12 Issue 17 Pg. 2313-20 (Dec 03 1998) ISSN: 0269-9370 [Print] England
• PMID: 9863874 (Publication Type: Clinical Trial, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-HIV Agents
• HIV Protease Inhibitors
• Indinavir
• Saquinavir
• Ritonavir

Topics

• AIDS-Related Opportunistic Infections (prevention & control)
• Adult
• Anti-HIV Agents (therapeutic use)
• CD4 Lymphocyte Count
• Cohort Studies
• Disease Progression
• Female
• Follow-Up Studies
• HIV Infections (drug therapy, immunology, mortality)
• HIV Protease Inhibitors (therapeutic use)
• Humans
• Indinavir (adverse effects, therapeutic use)
• Male
• Predictive Value of Tests
• Prospective Studies
• Risk Factors
• Ritonavir (adverse effects, therapeutic use)
• Saquinavir (adverse effects, therapeutic use)