title: Dysfunctional HDL and progression of atherosclerosis in HIV-1-infected and -uninfected adults.
abstract: BACKGROUND
  HDL function rather than absolute level may be a more accurate indicator for risk of developing atherosclerosis. Dysfunctional HDL has increased redox activity and reduced antioxidant properties, but it is unknown whether abnormal HDL function is associated with progression of atherosclerosis in HIV-1-infected subjects.
  
  
  RESULTS
  We retrospectively measured serum HDL function in 91 subjects from a prospective 3-year study of carotid artery intima-media thickness (CIMT), which enrolled triads of risk factor-matched persons that were HIV-1-uninfected (n=36) or HIV-1+ with (n=29) or without (n=26) protease inhibitor (PI)-based therapy for ≥ 2 years. HDL function was assessed using a biochemical assay that measures the oxidation of dihydrorhodamine 123 (DHR oxidation rate, DOR), in which higher DOR readout corresponds to dysfunctional HDL phenotype.There were no significant associations between DOR and HIV-1 infection. In univariate analysis of 55 HIV-1-infected subjects, greater waist circumference and lower serum HDL were significantly associated with higher baseline levels of DOR (p=0.01). These subjects had significant increases in levels of DOR over time (3 years) that were associated with white race (p=0.03), higher nadir CD4 count (p<0.001), and lower baseline CIMT (p<0.001). Lower baseline HDL levels, but not function of HDL (p>0.1) (DOR), were significantly associated (p=0.02) with progression of CIMT.
  
  
  CONCLUSIONS
  In a small matched cohort study of HIV-1-infected subjects who had a low cardiovascular risk profile, HDL function changed over time and was independently associated with anthropometric parameters of obesity but not with progression of CIMT.
authors.affiliation: Department of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
authors.forename: Theodoros
authors.initials: T
authors.lastname: Kelesidis
authors.forename: Otto O
authors.initials: OO
authors.lastname: Yang
authors.forename: Michelle A
authors.initials: MA
authors.lastname: Kendall
authors.forename: Howard N
authors.initials: HN
authors.lastname: Hodis
authors.forename: Judith S
authors.initials: JS
authors.lastname: Currier
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood* / Q000208:ethnology / Q000473:pathology / Q000821:virology; D018791:CD4 Lymphocyte Count; D002140:California; D002339:Carotid Arteries / Q000473:pathology / Q000821:virology; D059168:Carotid Intima-Media Thickness; D008076:Cholesterol, HDL / Q000097:blood*; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000097:blood* / Q000188:drug therapy / Q000208:ethnology / Q000821:virology; D016333:HIV Protease / Q000378:metabolism; D017320:HIV Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D015497:HIV-1; D006801:Humans; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D011446:Prospective Studies; D012189:Retrospective Studies; D012235:Rhodamines; D055105:Waist Circumference; D044465:White People
chemical_list: D008076:Cholesterol, HDL; D017320:HIV Protease Inhibitors; D012235:Rhodamines; C058319:dihydrorhodamine 123; D016333:HIV Protease