title: Elevated levels of high-sensitivity C-reactive protein and serum amyloid-A late after Kawasaki disease: association between inflammation and late coronary sequelae in Kawasaki disease.
abstract: BACKGROUND
  Coronary sequelae that persist after Kawasaki disease (KD) have been associated with obstructive changes of the lesions and coronary vascular events in adolescents and young adults. However, little is known about the association between sequelae late after KD and inflammatory markers, which are potential mediators and markers for atherogenesis.
  
  
  RESULTS
  Cross-sectional study was performed to test the hypothesis that coronary sequelae are associated with elevated levels of inflammatory markers in patients late after KD (mean time interval after the onset, 10 years, 10 months). Levels of high-sensitivity C-reactive protein (CRP), serum amyloid-A (SAA), interleukin-6, and soluble intercellular adhesion molecule-1 were measured in the 4 groups (n=80): the referent group (n=15) and KD subgroups with normal coronary arteries from the onset (n=27); with regressed aneurysms (n=18); and with coronary artery lesions, such as persistent aneurysms, stenosis, and occlusion (n=20). CRP levels were significantly elevated in a KD subgroup with coronary artery lesions compared with the referent or other KD subgroups, as analyzed by ANOVA and ANCOVA after adjustment for a confounding factor body mass index. Levels of CRP, SAA, and interleukin-6 were positively correlated. Stepwise regression and logistic regression analyses support the association between the persistence of coronary artery lesions and the levels of CRP and SAA.
  
  
  CONCLUSIONS
  Results demonstrate that the persistence of coronary lesions late after KD was independently associated with levels of CRP and SAA, suggesting that inflammation may be a novel functional aspect of coronary artery diseases late after KD.
authors.affiliation: Department of Pediatrics, Mie University School of Medicine, 2-174 Edobashi, Tsu City, Mie Prefecture, 514-8507, Japan. ymitani@clin.medic.mie-u.ac.jp
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Mitani
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Sawada
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Hayakawa
authors.forename: Kenzo
authors.initials: K
authors.lastname: Aoki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ohashi
authors.forename: Masahiko
authors.initials: M
authors.lastname: Matsumura
authors.forename: Kenji
authors.initials: K
authors.lastname: Kuroe
authors.forename: Hideto
authors.initials: H
authors.lastname: Shimpo
authors.forename: Masataka
authors.initials: M
authors.lastname: Nakano
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Komada
mesh_terms: D000293:Adolescent; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis*; D002648:Child; D003323:Coronary Aneurysm / Q000097:blood / Q000209:etiology; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000209:etiology; D003327:Coronary Disease / Q000097:blood / Q000209:etiology*; D023921:Coronary Stenosis / Q000097:blood / Q000209:etiology; D003430:Cross-Sectional Studies; D004198:Disease Susceptibility; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood* / Q000150:complications / Q000473:pathology; D000685:Serum Amyloid A Protein / Q000032:analysis*; D013997:Time Factors
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D000685:Serum Amyloid A Protein; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein