
ATV/r‐based regimens: durable virological suppression and good tolerability as switch strategy from NNRTI‐containing regimens in a real‐life cohort
Author(s) -
Michalik C,
Sönnerborg A,
Jansen K,
SvedhemJohansson V,
Harrer T,
Thalme A,
Eychenne J,
JimenezExposito M
Publication year - 2012
Publication title -
journal of the international aids society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.724
H-Index - 62
ISSN - 1758-2652
DOI - 10.7448/ias.15.6.18352
Subject(s) - discontinuation , tolerability , medicine , regimen , adverse effect , cohort , viral load , retrospective cohort study , human immunodeficiency virus (hiv) , immunology
Current therapeutic options for the treatment of HIV provide high rates of virological suppression and good tolerability. However, as long‐term treatment success has become a realistic goal, data evaluating the long‐term efficacy and safety of switching strategies become more needed. The purpose of this sub‐analysis is to describe the long‐term outcomes of ATV/r regimens after switching from combinations containing non‐nucleoside reverse transcriptase inhibitor (NNRTI) in a clinical setting. Non‐comparative, retrospective study including data from 3 European databases (France – DatAids, Germany‐KompNet, Sweden‐InfCare). Data from antiretroviral (ARV)‐experienced adults starting an ATV/r‐regimen between October 2004‐March 2007 were extracted every 6‐months (maximum follow‐up 5 years). Time to virological failure (VF) was analysed by the Kaplan‐Meier method. Reasons for discontinuation and safety data were also collected. Of 1294 patients analysed, 250 switched from a NNRTI‐based regimen. Patients were predominantly male (74%); median age 42 years (min, max: 23, 85); prior ARV exposure: median 5.0 years. At baseline (BL), 56% of patients had HIV‐1 RNA<500 c/mL and 31% had<50 c/mL; median (min, max) CD4 cell count: 388 (6, 1299) cells/mm3. After 3‐year follow‐up, the probability of not having VF was 79% (95% CI 65–88%) and 62% (95% CI 52%–70%) for patients with BL HIV‐1 RNA