title: Immunohistochemical study of apparently intact coronary artery in a child after Kawasaki disease.
abstract: BACKGROUND
  Coronary arterial lesions (CAL) due to Kawasaki disease (KD) often show progressive intimal hyperplasia even many years after the disease. However, most patients have no CAL after the acute phase, and it is an important issue whether or not coronary arteries without CAL have significant intimal hyperplasia, and whether or not there is the potential for this to progress to stenosis and/or atherosclerosis.
  
  
  METHODS
  The authors examined formalin-fixed specimens of the coronary arteries immunohistochemically, using antibodies against vascular growth factors (GFs), the receptors of transforming growth factor-beta (TbetaRs) and inducible nitric oxid synthesis (iNOS) in a KD patient without CAL, and also in four control patients: two with CAL due to KD and two without a history of KD.
  
  
  RESULTS
  Vascular endothelial GFs, Platelet-derived growth factor-A (PDGF-A) and TbetaRs were expressed in the vascular smooth muscle cells of all patients. PDGF-A, transforming Gfbeta1 and iNOS were expressed in the intimal smooth muscle cells of the KD but not the normal coronary artery without a history of KD. The number of TbetaR-II-positive cells were fewer than TbetaR-I-positive cells in the intima of CAL due to KD, but the number was of both almost same in the intima of coronary artery without CAL after KD and in the normal coronary.
  
  
  CONCLUSIONS
  The intact coronary artery 13 months after KD still showed the influence of the inflammation of KD. Although the authors speculate that the intimal proliferation will not continue beyond the acute phase, those patients may have a risk factor for atherosclerosis.
authors.affiliation: Department of Pediatrics, Tokyo Postal Services Agency Hospital, Tokyo, Japan. asuzuki@tth-japanpost.jp
authors.forename: Atsuko
authors.initials: A
authors.lastname: Suzuki
authors.forename: Sachiko
authors.initials: S
authors.lastname: Miyagawa-Tomita
authors.forename: Keiko
authors.initials: K
authors.lastname: Komatsu
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakazawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Fukaya
authors.forename: Kunizou
authors.initials: K
authors.lastname: Baba
authors.forename: Chikao
authors.initials: C
authors.lastname: Yutani
mesh_terms: D002675:Child, Preschool; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D003331:Coronary Vessels / Q000737:chemistry / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007223:Infant; D009080:Mucocutaneous Lymph Node Syndrome / Q000150:complications*; D019001:Nitric Oxide Synthase / Q000032:analysis; D052247:Nitric Oxide Synthase Type II; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D018125:Receptors, Transforming Growth Factor beta / Q000032:analysis; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D010982:Platelet-Derived Growth Factor; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II