title: Acute pericardial effusion representing the TNF-α-mediated severe inflammation but not the coronary artery outcome of Kawasaki disease.
abstract: OBJECTIVE
  To establish the optimal inflammation control of Kawasaki disease (KD), we investigated the clinical and pathophysiological basis of pericardial effusion (PE) during the acute phase of KD.
  
  
  METHODS
  Clinical and laboratory features of Japanese KD children with PE (PE group: n = 9) and without PE (non-PE group: n = 89) were studied retrospectively by using the medical records. Serum levels of soluble tumour necrosis factor receptor 1 (sTNFR1), interleukin 6 (IL-6), and vascular endothelial growth factor (VEGF) were assessed by enzyme-linked immunosorbent assays (ELISAs).
  
  
  RESULTS
  PE group patients had coronary artery lesions (CALs) more frequently than non-PE group patients during the acute phase of KD (33% vs. 5.6%, p = 0.024). PE patients also showed lower levels of haemoglobin (p < 0.01) and serum albumin (p < 0.01) and higher platelet counts (p = 0.013) than non-PE patients. The proportion of neurological symptoms, but not other manifestations, in the PE group was higher than in the non-PE group (p = 0.022). All patients survived free from coronary artery aneurisms. Serum levels of sTNFR1, but not the other cytokines, in the PE group were higher than those in the non-PE group (p < 0.001). The sTNFR1 levels correlated positively with C-reactive protein (CRP) (r = 0.30, p = 0.019) or total bilirubin (r = 0.40, p < 0.01) levels.
  
  
  CONCLUSIONS
  Acute PE in KD patients indicated the severity of TNF-mediated vascular inflammation and concurrent CALs. According to the progression, these patients might need more targeted therapy of anti-inflammation for a better coronary outcome.
authors.affiliation: Department of Paediatrics, Yamaguchi University Graduate School of Medicine , Ube , Japan.
authors.forename: S
authors.initials: S
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Hasegawa
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Matsubara
authors.forename: M
authors.initials: M
authors.lastname: Shimomura
authors.forename: M
authors.initials: M
authors.lastname: Okuda
authors.forename: T
authors.initials: T
authors.lastname: Ichiyama
authors.forename: S
authors.initials: S
authors.lastname: Ohga
mesh_terms: D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D003323:Coronary Aneurysm / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006454:Hemoglobins; D006801:Humans; D007223:Infant; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood* / Q000150:complications; D010490:Pericardial Effusion / Q000097:blood* / Q000000981:diagnostic imaging / Q000209:etiology; D010976:Platelet Count; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D012189:Retrospective Studies; D012709:Serum Albumin; D014463:Ultrasonography; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D006454:Hemoglobins; C508600:IL6 protein, human; D015850:Interleukin-6; D047888:Receptors, Tumor Necrosis Factor, Type I; D012709:Serum Albumin; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D002097:C-Reactive Protein