title: Circulating platelet-neutrophil aggregates play a significant role in Kawasaki disease.
abstract: BACKGROUND
  Circulating platelet-neutrophil aggregates play a crucial role in amplifying acute inflammation and could promote adverse effects involving vascular injury. The aim of this study was to evaluate the role of platelet-neutrophil aggregates in Kawasaki disease (KD).
  
  
  RESULTS
  Forty patients with KD (30 intravenous immunoglobulin [IVIG] responders and 10 IVIG non-responders), 7 febrile patients with bacterial infections, and 9 normal volunteers were analyzed. Thirty-three patients with KD were treated with IVIG, and 7 were treated with IVIG plus prednisolone. We evaluated the rate of platelet-neutrophil aggregates and measured the platelet factor 4 (PF4) and β-thromboglobulin (β-TG) levels. The rate of platelet-neutrophil aggregates was significantly higher in patients with KD than those with bacterial infection and normal volunteers. The rate of platelet-neutrophil aggregates was significantly higher in patients with coronary artery abnormalities (CAA) than in those without CAA, and was correlated with PF4 and β-TG levels in patients with KD. Comparing time-course analysis, the rate of platelet-neutrophil aggregates was significantly decreased in patients treated with IVIG plus prednisolone than in those treated with IVIG alone.
  
  
  CONCLUSIONS
  The findings demonstrate that platelet-neutrophil aggregates are significantly present in higher rates and are closely related to pathological developments of CAA in KD. Additional prednisolone treatment for patients in the acute phase of KD could suppress platelet-neutrophil aggregates, indicating that platelet-neutrophil aggregates would inhibit amplified reciprocal vascular inflammatory activation.
authors: Department of Pediatrics, Kagoshima University Graduate School of Medical and Dental Sciences.
authors: Kentaro
authors: K
authors: Ueno
authors: Yuichi
authors: Y
authors: Nomura
authors: Yasuko
authors: Y
authors: Morita
authors: Taisuke
authors: T
authors: Eguchi
authors: Kiminori
authors: K
authors: Masuda
authors: Yoshifumi
authors: Y
authors: Kawano
mesh_terms: D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000473:pathology*; D002675:Child, Preschool; D003331:Coronary Vessels / Q000473:pathology; D004351:Drug Resistance; D005260:Female; D005334:Fever / Q000188:drug therapy / Q000209:etiology; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D007223:Infant; D008297:Male; D009080:Mucocutaneous Lymph Node Syndrome / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy; D009504:Neutrophils / Q000473:pathology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D010978:Platelet Factor 4 / Q000097:blood; D011239:Prednisolone / Q000627:therapeutic use; D014463:Ultrasonography; D001620:beta-Thromboglobulin / Q000032:analysis
chemical_list: D016756:Immunoglobulins, Intravenous; D007166:Immunosuppressive Agents; C061615:PPBP protein, human; D010975:Platelet Aggregation Inhibitors; D001620:beta-Thromboglobulin; D010978:Platelet Factor 4; D011239:Prednisolone; D001241:Aspirin