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Changes in biomarkers of cardiovascular risk after a switch to abacavir in HIV‐1‐infected individuals receiving combination antiretroviral therapy
Author(s) -
Kristoffersen US,
Kofoed K,
Kronborg G,
Benfield T,
Kjaer A,
Lebech AM
Publication year - 2009
Publication title -
hiv medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.53
H-Index - 79
eISSN - 1468-1293
pISSN - 1464-2662
DOI - 10.1111/j.1468-1293.2009.00733.x
Subject(s) - medicine , abacavir , antiretroviral therapy , human immunodeficiency virus (hiv) , tenofovir , oncology , virology , viral load
Objectives To investigate, using a longitudinal design, whether biomarkers of cardiovascular risk change after a switch to an abacavir (ABC)‐containing regimen in HIV‐1‐infected individuals already receiving combination antiretroviral therapy (ART). Methods Thirty‐five HIV‐1‐infected individuals who switched ART to an ABC‐containing regimen were identified. Twenty‐two HIV‐1‐infected individuals who switched ART from and to a non‐ABC‐containing regimen served as controls. Plasma concentrations of soluble vascular cell adhesion molecule 1 (sVCAM‐1), soluble intercellular adhesion molecule 1 (sICAM‐1), matrix metallopeptidase 9 (MMP9), myeloperoxidase (MPO) and high sensitivity C‐reactive protein (hs‐CRP) were measured in blood samples before the switch in ART, and 3 months and 12 months afterwards. Log 10 ‐transformed data were compared with paired t ‐tests. Results Median MMP9 increased from 45.5 to 64.4 μg/mL after 3 months of ABC exposure ( P =0.011) and remained increased after 12 months (64.2 μg/mL; P =0.013). MPO increased from median 8.8 to 10.4 μg/mL ( P =0.036) after 3 months of ABC exposure but was not increased after 12 months of exposure (9.1 μg/mL). hs‐CRP increased from 3.3 to 4.2 μg/mL after 3 months ( P =0.031) but was not increased after 12 months of exposure (2.8 μg/mL). Neither sVCAM‐1 nor sICAM‐1 changed after the initiation of ABC. No changes were observed in the control group. Conclusions MMP9, MPO and hs‐CRP all increased after a switch in ART to an ABC‐containing regimen. This indicates increased cardiovascular risk in viral load‐suppressed HIV‐1‐infected individuals switching to ABC and proposes a proinflammatory potential as the underlying pathogenetic mechanism.