Cargando…

Viral load responses to HAART is an independent predictor of a new AIDS event in late stage HIV infected patients: prospective cohort study

BACKGROUND: A sizeable number of HIV-infected patients receiving HAART do not maintain prolonged virologic suppression. We evaluated long-term HIV viral load (VL) responses to HAART as a risk factor for AIDS events (AE) that is independent of CD4 responses. METHODS: A cohort of patients with pre-the...

Descripción completa

Detalles Bibliográficos
Autores principales: Kazanjian, Powel, Wei, Wei, Brown, Morton, Gandhi, Tejal, Amin, Kamal
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298340/
https://www.ncbi.nlm.nih.gov/pubmed/16262894
http://dx.doi.org/10.1186/1479-5876-3-40
Descripción
Sumario:BACKGROUND: A sizeable number of HIV-infected patients receiving HAART do not maintain prolonged virologic suppression. We evaluated long-term HIV viral load (VL) responses to HAART as a risk factor for AIDS events (AE) that is independent of CD4 responses. METHODS: A cohort of patients with pre-therapy CD4 < 200/mm(3 )who had CD4 and VL measurements for > one year after receiving HAART at a university clinic were prospectively enrolled. Cox proportional multivariate regression model was used to determine whether CD4 and VL responses were independently associated with new AE. RESULTS: The patient (N = 214) mean baseline CD4 = 92/mm(3), VL = 219,000 c/mL and follow-up duration 42.3 months (range 13–72 months). A new AE occurred in 56 patients; CD4 cell count response to HAART that remained < 200/mm(3 )throughout the study period was a significant risk factor for new AE (RR = 9.7–12.5; p < 0.001). Similarly, VL responses that remained > 5,000 c/mL during this period was also a significant risk factor (RR = 6.7–12.8; p = 0.001) that was independent of CD4 response adjusted for <> 200/mm(3). CONCLUSION: Maintaining adequate long-term virologic responses to HAART provides a clinical benefit independent of CD4 responses.