title: Protease inhibitor-based HAART, HDL, and CHD-risk in HIV-infected patients.
abstract: OBJECTIVE
  To study the effects of HIV-infection and protease inhibitor (PI)-based highly active anti-retroviral therapy (HAART) on the lipid and high-density lipoprotein (HDL) subpopulation profile and to relate the changes to coronary heart disease (CHD)-risk.
  
  
  METHODS
  The lipid and HDL subpopulation profiles of HIV-positive subjects (n = 48) were studied prospectively by comparing pre- and post-PI-HAART data as well as cross-section by comparing the profiles to HIV-negative subjects with (n = 96) and without CHD (n = 96).
  
  
  RESULTS
  HIV-infected HAART-naïve subjects had lower concentrations of low-density lipoprotein cholesterol (LDL-C) and HDL-C and higher concentration of triglycerides (TG) than healthy controls. After receiving PI-based HAART, LDL-C and TG concentrations increased, while HDL-C concentrations remained unchanged. The HDL subpopulation profiles of HAART-naïve HIV-positive patients were significantly different from those of healthy controls and were similar to those with CHD. Moreover, the HDL subpopulation profile changed unfavorably after PI-based HAART, marked with increased concentrations of the small, lipid-poor pre-beta-1 HDL (32% or 3.9 mg/dl; p < 0.001), and decreased concentration of the large, cholesterol-rich alpha-1 HDL (9% or 1 mg/dl ns).
  
  
  CONCLUSIONS
  An already unfavorable lipid and HDL subpopulation profile of HIV-positive HAART-naïve subjects further deteriorated after receiving PI-based treatment, which may cause increased CHD-risk in these subjects.
authors.affiliation: Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Center on Aging, Tufts University, Boston, MA 02111, USA. bela.asztalos@tufts.edu
authors.forename: Bela F
authors.initials: BF
authors.lastname: Asztalos
authors.forename: Ernst J
authors.initials: EJ
authors.lastname: Schaefer
authors.forename: Katalin V
authors.initials: KV
authors.lastname: Horvath
authors.forename: Caitlin E
authors.initials: CE
authors.lastname: Cox
authors.forename: Sally
authors.initials: S
authors.lastname: Skinner
authors.forename: Jul
authors.initials: J
authors.lastname: Gerrior
authors.forename: Sherwood L
authors.initials: SL
authors.lastname: Gorbach
authors.forename: Christine
authors.initials: C
authors.lastname: Wanke
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood* / Q000150:complications; D018450:Disease Progression; D005260:Female; D006678:HIV / Q000276:immunology*; D015483:HIV Antibodies / Q000276:immunology*; D015658:HIV Infections / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011480:Protease Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D012307:Risk Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015483:HIV Antibodies; D011480:Protease Inhibitors; D014280:Triglycerides