title: High plasma leptin levels confer increased risk of atherosclerosis in women with systemic lupus erythematosus, and are associated with inflammatory oxidised lipids.
abstract: BACKGROUND
  Patients with systemic lupus erythematosus (SLE) are at increased risk of atherosclerosis, even after accounting for traditional risk factors. High levels of leptin and low levels of adiponectin are associated with both atherosclerosis and immunomodulatory functions in the general population.
  
  
  OBJECTIVE
  To examine the association between these adipokines and subclinical atherosclerosis in SLE, and also with other known inflammatory biomarkers of atherosclerosis.
  
  
  METHODS
  Carotid ultrasonography was performed in 250 women with SLE and 122 controls. Plasma leptin and adiponectin levels were measured. Lipoprotein a (Lp(a)), oxidised phospholipids on apoB100 (OxPL/apoB100), paraoxonase, apoA-1 and inflammatory high-density lipoprotein (HDL) function were also assessed.
  
  
  RESULTS
  Leptin levels were significantly higher in patients with SLE than in controls (23.7±28.0 vs 13.3±12.9 ng/ml, p<0.001). Leptin was also higher in the 43 patients with SLE with plaque than without plaque (36.4±32.3 vs 20.9±26.4 ng/ml, p=0.002). After multivariate analysis, the only significant factors associated with plaque in SLE were leptin levels in the highest quartile (≥29.5 ng/ml) (OR=2.8, p=0.03), proinflammatory HDL (piHDL) (OR=12.8, p<0.001), age (OR=1.1, p<0.001), tobacco use (OR=7.7, p=0.03) and hypertension (OR=3.0, p=0.01). Adiponectin levels were not significantly associated with plaque in our cohort. A significant correlation between leptin and piHDL function (p<0.001), Lp(a) (p=0.01) and OxPL/apoB100 (p=0.02) was also present.
  
  
  CONCLUSIONS
  High leptin levels greatly increase the risk of subclinical atherosclerosis in SLE, and are also associated with an increase in inflammatory biomarkers of atherosclerosis such as piHDL, Lp(a) and OxPL/apoB100. High leptin levels may help to identify patients with SLE at risk of atherosclerosis.
authors.affiliation: Division/Department of Rheumatology, UCLA David Geffen School of Medicine, Los Angeles, California, USA. mmcmahon@mednet.ucla.edu
authors.forename: Maureen
authors.initials: M
authors.lastname: McMahon
authors.forename: Brian J
authors.initials: BJ
authors.lastname: Skaggs
authors.forename: Lori
authors.initials: L
authors.lastname: Sahakian
authors.forename: Jennifer
authors.initials: J
authors.lastname: Grossman
authors.forename: John
authors.initials: J
authors.lastname: FitzGerald
authors.forename: Nagesh
authors.initials: N
authors.lastname: Ragavendra
authors.forename: Christina
authors.initials: C
authors.lastname: Charles-Schoeman
authors.forename: Marissa
authors.initials: M
authors.lastname: Chernishof
authors.forename: Alan
authors.initials: A
authors.lastname: Gorn
authors.forename: Joseph L
authors.initials: JL
authors.lastname: Witztum
authors.forename: Weng Kee
authors.initials: WK
authors.lastname: Wong
authors.forename: Michael
authors.initials: M
authors.lastname: Weisman
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Wallace
authors.forename: Antonio
authors.initials: A
authors.lastname: La Cava
authors.forename: Bevra H
authors.initials: BH
authors.lastname: Hahn
mesh_terms: D054392:Adipokines / Q000097:blood; D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000209:etiology*; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging; D004812:Epidemiologic Methods; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D020738:Leptin / Q000097:blood*; D008055:Lipids / Q000097:blood; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications*; D008875:Middle Aged; D010084:Oxidation-Reduction; D014463:Ultrasonography
chemical_list: D054392:Adipokines; D015415:Biomarkers; D018836:Inflammation Mediators; D020738:Leptin; D008055:Lipids