title: Imbalance of peroxisome proliferator-activated receptor gamma and adiponectin predisposes Kawasaki disease patients to developing atherosclerosis.
abstract: BACKGROUND
  It remains controversial whether Kawasaki disease (KD) is a risk factor for the onset of atherosclerosis. An imbalance of peroxisome proliferator-activated receptor γ (PPARγ) and adiponectin appears to play a role in the onset of atherosclerosis in adults, and we therefore examined PPARγ mRNA expression and adiponectin profiles in the peripheral white blood cells obtained from KD patients.
  
  
  METHODS
  A total of 50 subjects were studied: nine patients with acute KD, 20 patients with convalescent KD, and 21 age-matched controls. The gene expression of PPARγ, monocyte chemoattractant protein-1, and CC chemokine receptor 2 present in the blood were quantified. The relative gene expression, adiponectin levels, and the three adiponectin isoforms were compared among the subjects.
  
  
  RESULTS
  The abundance of PPARγ and CC chemokine receptor 2 mRNA was significantly increased in convalescent KD patients. The monocyte chemoattractant protein-1 level was also increased in convalescent KD patients. The level of high-molecular-weight adiponectin was significantly lower in convalescent patients compared to controls. The PPARγ transcription levels negatively correlated with apolipoprotein A-I levels in acute KD patients.
  
  
  CONCLUSIONS
  The transcript abundance of PPARγ and low levels of high-molecular-weight adiponectin in KD patients may have important clinical implications on the development of premature atherosclerosis. Because the potential risk for developing atherosclerosis has not yet been verified, long-term observation is important, even in convalescent KD patients without coronary artery lesions.
authors.affiliation: Department of Pediatrics, Juntendo University School of Medicine, Tokyo, Japan. fukunaga@juntendo.ac.jp
authors.forename: Hideo
authors.initials: H
authors.lastname: Fukunaga
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kishiro
authors.forename: Katsumi
authors.initials: K
authors.lastname: Akimoto
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Ohtsuka
authors.forename: Satoru
authors.initials: S
authors.lastname: Nagata
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Shimizu
mesh_terms: D000208:Acute Disease; D052242:Adiponectin / Q000235:genetics*; D000293:Adolescent; D017668:Age of Onset; D050197:Atherosclerosis / Q000175:diagnosis / Q000453:epidemiology* / Q000235:genetics*; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics; D002648:Child; D002675:Child, Preschool; D002908:Chronic Disease; D005260:Female; D005786:Gene Expression Regulation; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D006801:Humans; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics*; D047495:PPAR gamma / Q000235:genetics*; D011237:Predictive Value of Tests; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric
chemical_list: D052242:Adiponectin; D018932:Chemokine CCL2; D005819:Genetic Markers; D047495:PPAR gamma; D012333:RNA, Messenger