Abstract

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Virologic and immunologic responses to efavirenz or boosted lopinavir as first therapy for patients with HIV in the Swiss HIV Cohort Study (SHCS)

H.C. Bucher1,2, J. Young1, H. Günthard3, M. Rickenbach4, C.A. Fux5, B. Hirschel6, M. Cavassini7, P. Vernazza8, E. Bernasconi9, M. Battegay2, and the Swiss HIV Cohort Study

1Basel Institute for Clinical Epidemiology & Biostatistics, University Hospital Basel, Basel, Switzerland, 2Division of Infectious Diseases and Hospital Hygiene, University Hospital Basel, Basel, Switzerland, 3Divsion of Infectious Diseases and Hospital Epidemiology, University Hospital Zurich, Zurich, Switzerland, 4Swiss HIV Cohort Study Data Centre, University Hospital Lausanne, Lausanne, Switzerland, 5Division of Infectious Diseases, Insel Spital Berne, Berne, Switzerland, 6Division of Infectious Diseases, University Hospital Geneva, Geneva, Switzerland, 7Division of Infectious Diseases, University Hospital Lausanne, Lausanne, Switzerland, 8Division of Infectious Diseases, Cantonal Hospital St. Gallen, St. Gallen, Switzerland, 9Division of Infectious Diseases, Regional Hospital Lugano, Lugano, Switzerland

Background: Previous observational studies comparing first line therapy with efavirenz (EFV) or lopinavir(LPV/r) gave different results to those of the largest randomised trial (ACTG 5142). We investigate the relative benefits of EFV and LPV/r as first therapy in the SHCS.
Methods: We analyse data from all naive patients starting either EFV or LPV/r with lamivudine and zidovudine. We fit proportional hazards models and then add an interaction term to each model to show how the relative effect of therapy is modified by the CD4 cell count when starting therapy.
Results: 660 patients started EFV (median follow up 4.5 years) and 541 started LPV/r (median follow up 3.1 years). Virologic failure was defined based on the 2008 DHHS guidelines definition. The adjusted hazard ratio (HR, 95% CI) of virologic failure for EFV compared to LPV/r was 0.64 (0.51 to 0.80). Adding an interaction term shows that for each 100/microL lower CD4 cell count when starting therapy, this HR for therapy is then multiplied by a factor of 1.00 (0.90 to 1.12). Immune recovery was defined as the CD4 increase achieved by ≥80% of patients with viral suppression according to EuroSIDA statistics cross-classified by CD4 cell count when starting therapy and number of years on therapy. The adjusted HR shows an advantage for EFV therapy over LPV/r (0.65, 0.51 to 0.83). However adding an interaction term shows that for each 100/microL lower CD4 cell count when starting therapy, this HR for therapy is then multiplied by a factor of 1.32 (1.16 to 1.50).
Conclusions: Patients on EFV compared to LPV/r have a lower risk of virologic failure and this risk seems independent of their CD4 count when starting therapy. Patients on EFV also appear more likely to maintain an expected rate of CD4 cell increase unless they start therapy with an advanced infection.

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