title: Cardiovascular disease and serum defensin levels in systemic lupus erythematosus.
abstract: OBJECTIVE
  To analyse if defensins, immunomodulatory peptides involved in angiogenesis and elevated in the sera of systemic lupus erythematosus (SLE) patients, relate to cardiovascular disease in SLE.
  
  
  METHODS
  Serum levels of the defensins human beta defensin 2 (hBD2) and human neutrophil peptide (HNP) of 72 SLE patients were determined by ELISA at baseline. Cardiovascular risk factors and the occurrence of cardiovascular events (CVE: stroke, claudication, angina pectoris, myocardial infarction) were recorded over 6 years. Intima media thickness of the carotid arteries (CIMT) was measured by ultrasound in 42 patients at baseline and at 4 years. Normally distributed log-transformed defensin levels (log-hBD2 and log-HNP) were used for statistical analysis.
  
  
  RESULTS
  SLE patients who experienced a CVE had significantly higher log-hBD2 values and a likelihood-ratio for CVE of 2.23 when levels increased above 3.3 log(ng/ml). Using binary logistic regression analysis, log-hBD2 significantly contributed to a model also incorporating the number of traditional cardiovascular risk factors (dyslipidemia, hypertension, positive family history, age, smoking) as explanatory variables for the incidence of cardiovascular events. Moreover, SLE patients with progressive CIMT showed increased log-hBD2 and log-HNP values. Both defensin-levels also showed some correlation to the plaque stadium at baseline (hBD2: r2 0.10; HNP r2 0.12). Neither log-hBD2 nor log-HNP were correlated to traditional cardiovascular risk factors.
  
  
  CONCLUSIONS
  HNP and especially hBD2 may be indicators of progressive cardiovascular disease in SLE.
authors.affiliation: Heinrich-Heine-University, Department of Endocrinology, Diabetology and Rheumatology, Düsseldorf, Germany. stefa.vordenbaeumen@med.uni-duesseldorf.de
authors.forename: S
authors.initials: S
authors.lastname: Vordenbäumen
authors.forename: O
authors.initials: O
authors.lastname: Sander
authors.forename: E
authors.initials: E
authors.lastname: Bleck
authors.forename: M
authors.initials: M
authors.lastname: Schneider
authors.forename: R
authors.initials: R
authors.lastname: Fischer-Betz
mesh_terms: D000787:Angina Pectoris / Q000097:blood / Q000453:epidemiology / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000097:blood* / Q000453:epidemiology / Q000276:immunology*; D023082:Defensins / Q000097:blood*; D018450:Disease Progression; D050171:Dyslipidemias / Q000097:blood / Q000453:epidemiology / Q000276:immunology; D005260:Female; D006801:Humans; D007383:Intermittent Claudication / Q000097:blood / Q000453:epidemiology / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000453:epidemiology / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000453:epidemiology / Q000276:immunology; D012307:Risk Factors; D020521:Stroke / Q000097:blood / Q000453:epidemiology / Q000276:immunology
chemical_list: D015415:Biomarkers; D023082:Defensins