title: Plasma vitamin D levels and inflammation in the aortic wall of patients with coronary artery disease with and without inflammatory rheumatic disease.
abstract: OBJECTIVE
  Vitamin D modulates inflammation, and this may explain the observed associations between vitamin D status and disorders driven by systemic inflammation, such as coronary artery disease (CAD) and inflammatory rheumatic diseases (IRDs). The aims of this study were to assess vitamin D status in patients with CAD alone and in patients with CAD and IRD, and to explore potential associations between vitamin D status and the presence of mononuclear cell infiltrates (MCIs) in the aortic adventitia of these patients.
  
  
  METHODS
  Plasma levels of 25-hydroxyvitamin D3[(25(OH)D3] were determined by radioimmunoassay and 1,25-dihydroxyvitamin D3[1,25(OH)2D3] by enzyme immunoassay in the 121 patients from the Feiring Heart Biopsy Study (FHBS) who had available histology data on adventitial MCIs; 53 of these had CAD alone and 68 had CAD and IRD.
  
  
  RESULTS
  In the crude analysis, vitamin D levels were similar in CAD patients with and without IRD. After adjustment for potential confounders, IRD was associated with an increase of 8.8 nmol/L [95% confidence interval (CI) 1.0-16.6; p = 0.027] in 25(OH)D3and an increase of 18.8 pmol/L (95% CI 4.3-33.3; p = 0.012) in 1,25(OH)2D3, while MCIs in the aortic adventitia were associated with lower levels of 1,25(OH)2D3(β = -18.8, 95% CI -33.6 to -4.0; p = 0.014).
  
  
  CONCLUSIONS
  IRD was associated with higher levels of both 25(OH)D3and 1,25(OH)2D3. These findings argue against the hypothesis that patients with high systemic inflammatory burden (CAD+IRD) should have lower vitamin D levels than those with less inflammation (CAD only). Of note, when controlled for potential confounders, low 1,25(OH)2D3levels were associated with adventitial aortic inflammation.
authors.affiliation: a Department of Pathology , Innlandet Hospital Trust , Lillehammer , Norway.|b Institute of Clinical Medicine , University of Oslo , Oslo , Norway.
authors.forename: I
authors.initials: I
authors.lastname: Oma
authors.affiliation: c Department of Health, Technology and Society , Norwegian University of Science and Technology , Gjøvik , Norway.
authors.forename: J K
authors.initials: JK
authors.lastname: Andersen
authors.affiliation: d Department of Medical Biochemistry , Oslo University Hospital , Oslo , Norway.
authors.forename: T
authors.initials: T
authors.lastname: Lyberg
authors.affiliation: e Department of Rheumatology, Dermatology and Infectious Diseases , University of Oslo , Oslo , Norway.
authors.forename: Ø
authors.initials: Ø
authors.lastname: Molberg
authors.affiliation: f Department of Medical Biochemistry , Innlandet Hospital Trust , Lillehammer , Norway.
authors.forename: J E
authors.initials: JE
authors.lastname: Whist
authors.affiliation: g Oslo Centre for Biostatistics and Epidemiology, Research Support Services , Oslo University Hospital , Oslo , Norway.
authors.forename: M W
authors.initials: MW
authors.lastname: Fagerland
authors.affiliation: h University of North Norway , Tromsø , Norway.
authors.forename: S M
authors.initials: SM
authors.lastname: Almdahl
authors.affiliation: i Lillehammer Hospital for Rheumatic Diseases , Lillehammer , Norway.
authors.forename: I
authors.initials: I
authors.lastname: Hollan
mesh_terms: D063194:Adventitia / Q000276:immunology* / Q000473:pathology; D000368:Aged; D001011:Aorta / Q000276:immunology* / Q000473:pathology; D002112:Calcifediol / Q000097:blood*; D002117:Calcitriol / Q000097:blood*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood* / Q000150:complications / Q000276:immunology; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000276:immunology*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011863:Radioimmunoassay; D012216:Rheumatic Diseases / Q000097:blood* / Q000150:complications / Q000276:immunology
chemical_list: D002117:Calcitriol; D002112:Calcifediol