title: Clinical, virologic, and immunologic response to efavirenz-or protease inhibitor-based highly active antiretroviral therapy in a cohort of antiretroviral-naive patients with advanced HIV infection (EfaVIP 2 study).
abstract: OBJECTIVE
  To compare the clinical, immunologic, and virologic outcomes of efavirenz (EFV)-based versus protease inhibitor (PI)-based highly active antiretroviral therapy (HAART) in severely immunosuppressed HIV-1-infected patients.
  
  
  METHODS
  Retrospective observational cohort study.
  
  
  METHODS
  Responses were analyzed according to the intent-to-treat principle among antiretroviral-naive patients with < 100 CD4 cells/muL who started EFV (n = 92) or a PI (n = 218) plus 2 nucleoside reverse transcriptase inhibitors. The primary end point was time to treatment failure. Secondary end points were percentage of patients with a viral load < 400 copies/mL, time to virologic failure, time to CD4 lymphocyte count > 200 cells/microL, and incidence of opportunistic events or death.
  
  
  RESULTS
  The median baseline CD4 cell count and viral load were 34 cells/microL and 5.54 log10 copies/mL (EFV group) and 38 cells/microL and 5.40 log10 copies/mL (PI group). Time to treatment failure was shorter with a PI-based regimen than with an EFV-based regimen (adjusted relative hazard [RH] = 2.19, 95% confidence interval [CI]: 1.23-3.89). After 12 months of therapy, a significantly higher proportion of patients receiving EFV reached a viral load < 400 copies/mL (69.4 vs. 45.1%; P < 0.05). The probability of virologic failure was higher with a PI than with EFV (adjusted HR = 2.52, 95% CI: 1.14-5.61; P = 0.024). There was no difference in time to CD4 cell count > 200 cells/microL or in incidence of opportunistic events or death.
  
  
  CONCLUSIONS
  : In severely immunosuppressed, antiretroviral-naive, HIV-1-infected patients, treatment with an EFV-based regimen compared with a nonboosted PI-based regimen resulted in a superior virologic response with no difference in immunologic or clinical effectiveness.
authors.affiliation: HIV Unit, Hospital 12 de Octubre, Complutense University School of Medicine, Madrid, Spain. fpulido@palmedico.com
authors.forename: Federico
authors.initials: F
authors.lastname: Pulido
authors.forename: Jose R
authors.initials: JR
authors.lastname: Arribas
authors.forename: Jose M
authors.initials: JM
authors.lastname: Miró
authors.forename: María A
authors.initials: MA
authors.lastname: Costa
authors.forename: Juan
authors.initials: J
authors.lastname: González
authors.forename: Rafael
authors.initials: R
authors.lastname: Rubio
authors.forename: Jose M
authors.initials: JM
authors.lastname: Peña
authors.forename: Miguel
authors.initials: M
authors.lastname: Torralba
authors.forename: Montserrat
authors.initials: M
authors.lastname: Lonca
authors.forename: Alicia
authors.initials: A
authors.lastname: Lorenzo
authors.forename: Concepcion
authors.initials: C
authors.lastname: Cepeda
authors.forename: Juan J
authors.initials: JJ
authors.lastname: Vázquez
authors.forename: Jose M
authors.initials: JM
authors.lastname: Gatell
mesh_terms: D000328:Adult; D000480:Alkynes; D023241:Antiretroviral Therapy, Highly Active; D048588:Benzoxazines; D018791:CD4 Lymphocyte Count; D015331:Cohort Studies; D003521:Cyclopropanes; D004334:Drug Administration Schedule; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology; D017320:HIV Protease Inhibitors / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D010078:Oxazines / Q000627:therapeutic use*; D012189:Retrospective Studies; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use*
chemical_list: D000480:Alkynes; D048588:Benzoxazines; D003521:Cyclopropanes; D017320:HIV Protease Inhibitors; D010078:Oxazines; D018894:Reverse Transcriptase Inhibitors; C098320:efavirenz