title: The apolipoprotein E2 isoform is associated with accelerated onset of coronary artery disease in systemic lupus erythematosus.
abstract: BACKGROUND
  Systemic lupus erythematosus (SLE) is a highly prevalent autoimmune disease and coronary artery disease (CAD) is a complication of SLE which is often crucial for the patient's prognosis. It is hypothesized that apolipoprotein E (Apo E), which is involved in cholesterol metabolism, might play a role in this process.
  
  
  METHODS
  Patients with SLE registered at the University of Toronto Lupus Clinic who had DNA available for study had their Apo E genotype determined. Each case was assessed for the presence of CAD, and Apo E allele frequencies in patients with SLE were compared with data from the general population. Age at onset and disease duration of CAD were also recorded and compared between groups.
  
  
  RESULTS
  DNA was stored from 152 patients, of whom 38 (25%) had CAD. There was no difference in the frequencies of the Apo E isoforms between SLE patients and the general population. Patients with the E2 allele developed CAD after a mean +/-SD of 6.0+/-1.9 yrs compared with 14.5+/-5.4 yrs in those with E3/3 (p<0.01).
  
  
  CONCLUSIONS
  The distribution of Apo E genotypes in SLE is not significantly different from that of the North American population. In SLE, Apo E2 was associated with a more rapid development of CAD. Therefore, Apo E2 might interact with other disease-related factors to accelerate the onset of CAD in some patients with SLE and as such might be an additional marker of risk in this population.
authors.affiliation: Laboratorio di Neurogenetica, CERC-IRCCS Santa Lucia, Rome, Italy and Dipartimento di Neuroscienze, Università di Roma "Tor Vergata", Rome, Italy. a.orlacchio@hsantalucia.it
authors.forename: Antonio
authors.initials: A
authors.lastname: Orlacchio
authors.forename: Ian N
authors.initials: IN
authors.lastname: Bruce
authors.forename: Proton
authors.initials: P
authors.lastname: Rahman
authors.forename: Toshitaka
authors.initials: T
authors.lastname: Kawarai
authors.forename: Giorgio
authors.initials: G
authors.lastname: Bernardi
authors.forename: Peter H
authors.initials: PH
authors.lastname: St George-Hyslop
authors.forename: Dafna D
authors.initials: DD
authors.lastname: Gladman
authors.forename: Murray B
authors.initials: MB
authors.lastname: Urowitz
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D053329:Apolipoprotein E2 / Q000737:chemistry* / Q000235:genetics*; D002784:Cholesterol / Q000378:metabolism; D003324:Coronary Artery Disease / Q000150:complications* / Q000175:diagnosis* / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006239:Haplotypes; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000175:diagnosis* / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D020033:Protein Isoforms
chemical_list: D053329:Apolipoprotein E2; D020033:Protein Isoforms; D002784:Cholesterol