Abacavir-based therapy does not affect biological mechanisms associated with cardiovascular dysfunction

• Published in: AIDS (London) Vol. 24; no. 3; pp. F1 - F9
• Main Authors: MARTINEZ, Esteban, LARROUSSE, María, PICH, Judit, GATELL, José M, PODZAMCZER, Daniel, PEREZ, Ignacio, GUTIERREZ, Félix, LONCA, Montserrat, BARRAGAN, Patricia, DEULOFEU, Ramón, CASAMITJANA, Roser, MALLOLAS, Josep
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 28.01.2010
• Subjects: Adenine - administration & dosage; Adenine - analogs & derivatives; Adult; AIDS/HIV; Anti-HIV Agents - administration & dosage; Anti-HIV Agents - adverse effects; Antibiotics. Antiinfectious agents. Antiparasitic agents; Antiviral agents; Biological and medical sciences; Biomarkers - blood; Cardiovascular Diseases - blood; Deoxycytidine - administration & dosage; Deoxycytidine - analogs & derivatives; Dideoxynucleosides - administration & dosage; Dideoxynucleosides - adverse effects; Drug Therapy, Combination; Emtricitabine; Female; HIV Infections - blood; HIV Infections - drug therapy; HIV Infections - virology; HIV-1; Human immunodeficiency virus; Human viral diseases; Humans; Infectious diseases; Lamivudine - administration & dosage; Lipids - blood; Male; Medical sciences; Middle Aged; Organophosphonates - administration & dosage; Pharmacology. Drug treatments; Reverse Transcriptase Inhibitors - administration & dosage; Reverse Transcriptase Inhibitors - adverse effects; Tenofovir; Treatment Outcome; Viral diseases; Viral diseases of the lymphoid tissue and the blood. Aids; Viral Load; tenofovir/emtricitabine; Purine nucleoside; Antiretroviral agent; RNA-directed DNA polymerase; Nucleotide analog; Tenofovir; Reverse transcriptase inhibitor; Nucleoside analog; Antiviral; Clinical trial; Pyrimidine nucleoside; Emtricitabine; Purine nucleotide; Acyclic nucleotide; Enzyme; Transferases; Enzyme inhibitor; Lamivudine; Organic phosphonate; simplification; abacavir/lamivudine; Nucleotidyltransferases; reverse transcriptase inhibitors; Treatment; Dysfunction; Dideoxynucleoside; Abacavir
• ISSN: 0269-9370; 1473-5571
• DOI: 10.1097/QAD.0b013e32833562c5

To assess the effects of initiating abacavir-containing therapy on plasma lipids and cardiovascular biomarkers. Sub-study of the BICOMBO study in which participants were randomized to switch their nucleoside backbone to either abacavir/lamivudine or tenofovir/emtricitabine. We assessed 48-week changes in fasting lipids and several biomarkers including serum high-sensitivity C-reactive protein (hsCRP), monocyte chemoattractant protein-1 (MCP-1), osteoprotegerin, interleukin (IL)-6, IL-10, tumor necrosis factor alpha (TNF-alpha), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), selectin E and P, adiponectin, insulin, and D-dimer in otherwise healthy, virologically suppressed HIV-infected patients randomly switched to abacavir/lamivudine or tenofovir/emtricitabine with no history of cardiovascular disease, no prior abacavir or tenofovir use, and no virological failure or AIDS during follow-up. Eighty (46 abacavir/lamivudine and 34 tenofovir/emtricitabine) patients were included. Baseline characteristics were similar between groups and between patients in the sub-study vs. those not. There were no significant differences in baseline lipids and markers between groups. Although total (6.5 vs. -6.7%, P < 0.0001) and low-density lipoprotein (LDL) (8.6 vs. -9.1%, P = 0.004) cholesterol increased significantly in the abacavir/lamivudine group relative to the tenofovir/emtricitabine group, we found no significant changes in the biomarkers: CRP (-3.9 vs. 0.0%), MCP-1 (5.9 vs. 4.0%), osteoprotegerin (5.1 vs. -2.8%), IL-6 (0.0 vs. 0.0%), IL-10 (0.0 vs. 0.0%), TNF-alpha (0.0 vs. 0.0%), ICAM-1 (6.6 vs. 5.2%), VCAM-1 (0.02 vs. -0.01%), selectin E (-0.4 vs. 7.8%), selectin P (4.6 vs. 12.6%), insulin (-2.5 vs. 8.8%), adiponectin (-2.2 vs. 15.4%), and D-dimer (0.0 vs. 0.0%) (P > or = 0.12 for all comparisons). Abacavir/lamivudine increased total and LDL cholesterol compared with tenofovir/emtricitabine, but it did not cause inflammation, endothelial dysfunction, insulin resistance, or hypercoagulability in virologically suppressed HIV-infected patients.