title: Impact of antiretroviral therapy interruption on plasma biomarkers of cardiovascular risk and lipids: 144-week final data from the STOPAR study.
abstract: OBJECTIVE
  The aim of the study was to investigate changes in plasma biomarkers of cardiovascular risk and lipids in a CD4-guided antiretroviral therapy interruption study.
  
  
  METHODS
  This was a substudy of a prospective, randomized, multicentre treatment interruption study. At months 12, 24 and 36, monocyte chemotactic protein-1 (MCP-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), interleukin-6 (IL-6), interleukin-8 (IL-8), soluble CD40 ligand (sCD40L), soluble P-selectin (sP-selectin), and tissue plasminogen activator (t-PA) were measured using a multiplex cytometric bead-based assay. Total cholesterol (total-c), high-density lipoprotein cholesterol (HDL-c) and triglycerides (TG) were determined using standard methods.
  
  
  RESULTS
  Fifty-four patients were included in the study [34 in the treatment continuation (TC) arm and 20 in the treatment interruption (TI) arm]. There were no differences at baseline between the groups, except in CD4 cell count, which was higher in the TI arm (P = 0.026), and MCP-1, which was higher in the TC arm (P = 0.039). MCP-1 and sVCAM-1 were increased relative to baseline at the three study time-points in the TI arm, with no changes in the TC arm. Soluble CD40L and sP-selectin were increased at month 36 in both arms, with a greater increase in the TI arm (P = 0.02). t-PA was increased in both arms at the three time-points. Total-c, HDL-c and low-density lipoprotein cholesterol (LDL-c) were decreased in the TI arm at the three time-points, with no changes in the total-c/HDL-c ratio. HIV viral load positively correlated with MCP-1 at months 12 and 24. Regression analysis showed a significant negative association of HDL-c with MCP-1 and sVCAM-1.
  
  
  CONCLUSIONS
  A significant increase in cardiovascular risk biomarkers persisting over the prolonged study period was seen in the TI arm. This factor may contribute to the increased cardiovascular risk observed in previous studies.
authors.affiliation: Infectious Disease Service, Bellvitge University Hospital, Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Olmo
authors.forename: M
authors.initials: M
authors.lastname: Saumoy
authors.forename: C
authors.initials: C
authors.lastname: Alonso-Villaverde
authors.forename: M
authors.initials: M
authors.lastname: Peñaranda
authors.forename: F
authors.initials: F
authors.lastname: Gutiérrez
authors.forename: J
authors.initials: J
authors.lastname: Romeu
authors.forename: M
authors.initials: M
authors.lastname: Larrousse
authors.forename: J
authors.initials: J
authors.lastname: Curto
authors.forename: P
authors.initials: P
authors.lastname: Domingo
authors.forename: J A
authors.initials: JA
authors.lastname: Oteo
authors.forename: A
authors.initials: A
authors.lastname: Vila
authors.forename: D
authors.initials: D
authors.lastname: Podzamczer
mesh_terms: D000328:Adult; D000368:Aged; D044966:Anti-Retroviral Agents / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D018791:CD4 Lymphocyte Count; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D016207:Cytokines / Q000097:blood*; D005260:Female; D005434:Flow Cytometry / Q000379:methods; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006801:Humans; D008055:Lipids / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012044:Regression Analysis; D013030:Spain; D019562:Viral Load
chemical_list: D044966:Anti-Retroviral Agents; D015415:Biomarkers; D016207:Cytokines; D008055:Lipids