title: LDL subclasses and lipoprotein-phospholipase A2 activity in suppressed HIV-infected patients switching to raltegravir: Spiral substudy.
abstract: OBJECTIVE
  To analyze the effect of switching the ritonavir-boosted protease inhibitor (PI/r) in a stable combined antiretroviral therapy (cART) regimen to raltegravir on low-density lipoprotein (LDL) particles, and lipoprotein-associated phospholipase A2 (Lp-PLA2).
  
  
  METHODS
  Substudy of a multicenter randomized trial that compared the efficacy of switching a PI/r to raltegravir-based cART in stable HIV-infected patients.
  
  
  METHODS
  LDL size and phenotype (by gel-gradient electrophoresis), Lp-PLA2 (by 2-thio-PAF [Cayman]), proprotein convertase subtilisin/kexin type 9 (PCSK9) (by ELISA), and standard lipid parameters were measured at baseline and week 48.
  
  
  RESULTS
  Eighty-one (PI/r n = 41 and raltegravir n = 40) patients were evaluated. No differences in baseline demographic and metabolic variables between arms were found except in apolipoprotein (Apo) B (p = 0.042). At week 48, total cholesterol (TC) (p < 0.001), LDL-c (p = 0.023), non-high density lipoprotein cholesterol non-high-density lipoprotein cholesterol (non-HDL-c) (p < 0.001), TC/HDL (p = 0.026), triglyceride (p < 0.001), Apo B (p < 0.001), Apo A-I (p = 0.004) and Lp (a) (p = 0.005) decreased in raltegravir arm compared to PI/r arm. At week 48, a shift from LDL phenotype B to the less atherogenic phenotype A was observed only in raltegravir arm (p < 0.001). LDL size increased (PI/r 2.1 nm, p = 0.019; raltegravir 3.8 nm, p = 0.001) and cholesterol content in small and dense LDL subfractions (LDL 4,5,6) decreased (PI/r p = 0.007, raltegravir p = 0.006) at week 48 in both arms. Total Lp-PLA2 activity (PI/r p = 0.037 and raltegravir p = 0.051) and PCSK9 plasma concentration decreased in both arms (PI/r p = 0.034 and raltegravir p < 0.001).
  
  
  CONCLUSIONS
  Switching a PI/r to a raltegravir-based cART in virologically suppressed HIV-infected patients was associated with an overall improvement in lipid profile, including a shift to a less atherogenic LDL phenotype.
authors.affiliation: HIV Unit, Infectious Disease Service, Bellvitge University Hospital, Bellvitge Biomedical Research Institute, C/ Feixa Llarga s/n., Hospitalet de Llobregat, 08907 Barcelona, Spain.
authors.forename: Maria
authors.initials: M
authors.lastname: Saumoy
authors.forename: José Luis
authors.initials: JL
authors.lastname: Sánchez-Quesada
authors.forename: Esteban
authors.initials: E
authors.lastname: Martínez
authors.forename: Josep Maria
authors.initials: JM
authors.lastname: Llibre
authors.forename: Esteban
authors.initials: E
authors.lastname: Ribera
authors.forename: Hernando
authors.initials: H
authors.lastname: Knobel
authors.forename: Josep Maria
authors.initials: JM
authors.lastname: Gatell
authors.forename: Bonaventura
authors.initials: B
authors.lastname: Clotet
authors.forename: Adrian
authors.initials: A
authors.lastname: Curran
authors.forename: Jordi
authors.initials: J
authors.lastname: Curto
authors.forename: Margarita
authors.initials: M
authors.lastname: Masó
authors.forename: Jordi
authors.initials: J
authors.lastname: Ordoñez-Llanos
authors.forename: Daniel
authors.initials: D
authors.lastname: Podzamczer
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism*; D000328:Adult; D000368:Aged; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D015658:HIV Infections / Q000097:blood / Q000188:drug therapy*; D017320:HIV Protease Inhibitors / Q000627:therapeutic use*; D006801:Humans; D008055:Lipids / Q000097:blood*; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011760:Pyrrolidinones / Q000008:administration & dosage*; D000068898:Raltegravir Potassium
chemical_list: D008078:Cholesterol, LDL; D017320:HIV Protease Inhibitors; D008055:Lipids; D008077:Lipoproteins, LDL; D011760:Pyrrolidinones; D000068898:Raltegravir Potassium; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase