title: Accumulation of advanced glycation endproducts in patients with systemic lupus erythematosus.
abstract: OBJECTIVE
  To investigate whether advanced glycation endproducts (AGEs) are increased in patients with systemic lupus erythematosus (SLE), and are related to atherosclerosis, which is accelerated in SLE, and its traditional and non-traditional disease-related risk factors.
  
  
  METHODS
  Fifty-five SLE patients with inactive disease and 55 age- and sex-matched controls were included. The amount of skin autofluorescence (AF), as a measure for the accumulation of AGEs, was assessed by measuring UV-A light excitation-emission matrices (AF-EEMS). Traditional risk factors and disease-related factors were recorded. Plasma levels of C-reactive protein (CRP), as a marker for systemic inflammation, were assessed. Intima-media thickness (IMT) of the common carotid artery was determined by ultrasound.
  
  
  RESULTS
  Skin AF-EEMS was increased in SLE patients as compared with controls (1.50 +/- 0.5 a.u. vs 1.28 +/- 0.4 a.u., P = 0.006). Regarding all included risk factors, univariate analyses in patients revealed that AF-EEMS was associated with age (r = 0.48, P < 0.001), IMT (r = 0.35, P = 0.01), creatinine (r = 0.29, P = 0.03), SLICC damage index (r = 0.29, P = 0.03) and disease duration (r = 0.32, P = 0.02). In multivariate analysis, age and disease duration were independent predictors of accumulation of AGEs in SLE (P < 0.001, P = 0.03, respectively).
  
  
  CONCLUSIONS
  AGEs are increased in SLE compared with controls. Our findings indicate that AGE accumulation is associated with disease duration and might contribute to the development of accelerated atherosclerosis in SLE and, therefore, could be used for assessment of risk for long-term vascular complications.
authors.affiliation: Department of Internal Medicine, Division of Clinical Immunology, University Medical Centre Groningen, Groningen, The Netherlands. k.de.leeuw@int.umcg.nl
authors.forename: K
authors.initials: K
authors.lastname: de Leeuw
authors.forename: R
authors.initials: R
authors.lastname: Graaff
authors.forename: R
authors.initials: R
authors.lastname: de Vries
authors.forename: R P
authors.initials: RP
authors.lastname: Dullaart
authors.forename: A J
authors.initials: AJ
authors.lastname: Smit
authors.forename: C G
authors.initials: CG
authors.lastname: Kallenberg
authors.forename: M
authors.initials: M
authors.lastname: Bijl
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000209:etiology / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D017536:Carotid Artery, Common / Q000473:pathology; D005260:Female; D005453:Fluorescence; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D012720:Severity of Illness Index; D012867:Skin / Q000378:metabolism*; D013997:Time Factors; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology
chemical_list: D015415:Biomarkers; D017127:Glycation End Products, Advanced