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Antiretroviral treatment response of HIV‐infected children after prevention of mother‐to‐child transmission in West Africa
Author(s) -
Ndondoki Camille,
Dicko Fatoumata,
Coffie Patrick Ahuatchi,
Eboua Tanoh Kassi,
Ekouevi Didier Koumavi,
Kouadio Kouakou,
Aka Addi Edmond,
Malateste Karen,
Dabis François,
AmaniBosse Clarisse,
Toure Pety,
Leroy Valériane
Publication year - 2014
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.17.1.18737
Subject(s) - medicine , pediatrics , regimen , cohort , medical record , antiretroviral treatment , proportional hazards model , transmission (telecommunications) , cohort study , retrospective cohort study , survival analysis , human immunodeficiency virus (hiv) , antiretroviral therapy , viral load , immunology , electrical engineering , engineering
Introduction We assessed the rate of treatment failure of HIV‐infected children after 12 months on antiretroviral treatment (ART) in the Paediatric IeDEA West African Collaboration according to their perinatal exposure to antiretroviral drugs for preventing mother‐to‐child transmission (PMTCT). Methods A retrospective cohort study in children younger than five years at ART initiation between 2004 and 2009 was nested within the pWADA cohort, in Bamako‐Mali and Abidjan‐Côte d’Ivoire. Data on PMTCT exposure were collected through a direct review of children’s medical records. The 12‐month Kaplan‐Meier survival without treatment failure (clinical or immunological) was estimated and their baseline factors studied using a Cox model analysis. Clinical failure was defined as the appearance or reappearance of WHO clinical stage 3 or 4 events or any death occurring within the first 12 months of ART. Immunological failure was defined according to the 2006 World Health Organization age‐related immunological thresholds for severe immunodeficiency. Results Among the 1035 eligible children, PMTCT exposure was only documented for 353 children (34.1%) and remained unknown for 682 (65.9%). Among children with a documented PMTCT exposure, 73 (20.7%) were PMTCT exposed, of whom 61.0% were initiated on a protease inhibitor‐based regimen, and 280 (79.3%) were PMTCT unexposed. At 12 months on ART, the survival without treatment failure was 40.6% in the PMTCT‐exposed group, 25.2% in the unexposed group and 18.5% in the children with unknown exposure status ( p =0.002). In univariate analysis, treatment failure was significantly higher in children unexposed (HR 1.4; 95% CI: 1.0–1.9) and with unknown PMTCT exposure (HR 1.5; 95% CI: 1.2–2.1) rather than children PMTCT‐exposed ( p =0.01). In the adjusted analysis, treatment failure was not significantly associated with PMTCT exposure ( p =0.15) but was associated with immunodeficiency (aHR 1.6; 95% CI: 1.4–1.9; p =0.001), AIDS clinical events (aHR 1.4; 95% CI: 1.0–1.9; p =0.02) at ART initiation and receiving care in Mali compared to Côte d’Ivoire (aHR 1.2; 95% CI: 1.0–1.4; p= 0.04). Conclusions Despite a low data quality, PMTCT‐exposed West African children did not have a poorer 12‐month response to ART than others. Immunodeficiency and AIDS events at ART initiation remain the main predictors associated with treatment failure in this operational context.

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