title: Early changes in inflammatory and pro-thrombotic biomarkers in patients initiating antiretroviral therapy with abacavir or tenofovir.
abstract: BACKGROUND
  Abacavir has been associated with an increased risk of acute myocardial infarction, but the pathogenic mechanisms remain unknown. We evaluated longitudinal changes in pro-atherosclerotic biomarkers in patients initiating abacavir or tenofovir.
  
  
  METHODS
  Consecutive patients initiating antiretroviral therapy (ART) with abacavir/lamivudine or tenofovir/emtricitabine were included. Plasma levels of high sensitivity C reactive protein (hsCRP), interleukin-6 (IL-6), intercellular adhesion molecule-1, vascular cell adhesion molecule-1 (sVCAM-1) and plasminogen activator inhibitor-1 (PAI-1) were measured at baseline and at different time points throughout 48 weeks. Comparisons were adjusted for age, sex, ART status at inclusion, viral load, lipodystrophy, Framingham score and hepatitis C virus co-infection status.
  
  
  RESULTS
  50 patients were analyzed, 28 initiating abacavir and 22 tenofovir. The endothelial biomarker sVCAM-1 declined significantly in both treatment groups. hsCRP tended to increase soon after starting therapy with abacavir, a trend that was not seen in those initiating tenofovir. IL-6 significantly increased only at week 24 from baseline in patients on abacavir (+225%, p < 0.01) although the differences were not significant between groups. The procoagulant biomarker PAI-1 plasma levels increased from baseline at week 12 (+57%; p = 0.017), week 24 (+72%; p = 0.008), and week 48 (+149%; p < 0.001) in patients on tenofovir, but differences between groups were not statistically significant.
  
  
  CONCLUSIONS
  Changes in biomarkers of inflammation, coagulation, and endothelial function are not different in viremic patients starting ART with abacavir/lamivudine or tenofovir/emtricitabine. These changes occur in the early phases of treatment and include anti- and pro-atherosclerotic effects with both drugs.
authors.affiliation: Infectious Diseases Unit, Hospital General Universitario de Elche, Department of Clinical Medicine, University Miguel Hernández, Elche, Alicante, Spain.
authors.forename: Sergio
authors.initials: S
authors.lastname: Padilla
authors.forename: Mar
authors.initials: M
authors.lastname: Masiá
authors.forename: Natalia
authors.initials: N
authors.lastname: García
authors.forename: Inmaculada
authors.initials: I
authors.lastname: Jarrin
authors.forename: Consuelo
authors.initials: C
authors.lastname: Tormo
authors.forename: Félix
authors.initials: F
authors.lastname: Gutiérrez
mesh_terms: D000225:Adenine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000328:Adult; D019380:Anti-HIV Agents / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000276:immunology; D003029:Coagulants / Q000097:blood / Q000276:immunology; D015224:Dideoxynucleosides / Q000009:adverse effects / Q000627:therapeutic use*; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology*; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D063065:Organophosphonates / Q000009:adverse effects / Q000627:therapeutic use*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood / Q000276:immunology; D000068698:Tenofovir; D013927:Thrombosis / Q000209:etiology / Q000276:immunology*; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood / Q000276:immunology; D000099227:Abacavir
chemical_list: D000225:Adenine; D019380:Anti-HIV Agents; D015415:Biomarkers; D002097:C-Reactive Protein; D003029:Coagulants; D015224:Dideoxynucleosides; D018836:Inflammation Mediators; D015850:Interleukin-6; D063065:Organophosphonates; D017395:Plasminogen Activator Inhibitor 1; D000068698:Tenofovir; D019010:Vascular Cell Adhesion Molecule-1; D000099227:Abacavir