Abstract
The major pathology of Kawasaki disease (KD) is systemic vasculitis that is caused by inflammatory cytokines. In KD, increased neutrophils are supposed to be responsible to the injury of coronary arterial endothelium by producing elastase. We studied the correlation between the serum levels of G-CSF and cardiac complication in KD to prove the involvement of G-CSF in stimulation of the proliferation of granulocytes and eventually causing coronary artery lesion. Thirty patients diagnosed as having KD (17 males and 13 females, aged 2 months to 5 years) were enrolled in this study. Gammaglobulin (400mg/kg/day for 5 consecutive days) and aspirin (30mg/kg/day) were administered to all. Ten patients exhibited transient mitral or aortic valve regurgitation and 6 had transient or persistent coronary artery dilatation. Blood samples were collected weekly. Serum levels of G-CSF ware monitored by ELISA assay. The mean serum G-CSF was 247.2±339.1 pg/ml in the first week, decreased to 18.3±49.4 pg/ml in the second week, to 14.2±26.5 pg/ml in the third week, and to 15.2±21.8 pg/ml in the fourth week of acute phase KD. Serum G-CSF in patients with coronary artery dilatation (400.5±194.3 pg/ml) was significantly higher than in patients without dilatation (125.0±97.8pg/ml) in the first week (p<0.05).Mean number of neutrophils in patients with coronary artery dilatation (8856±2916 /μl) was not significantly different from that in without dilatation (10006±3810/μl) in the first week. The present study revealed that serum G-CSF was significantly higher in patients with coronary artery dilatation than in patients without dilatation in the first week of KD. G-CSF may play an important role in coronary artery dilatation through activating neutrophil function or other unknown processes in acute phase KD.
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Samada, K., Igarashi, H., Shiraishi, H. et al. Serum Granulocyte Colony-stimulating Factor is Increased in Association with Coronary Artery Dilatation in Kawasaki Disease. Pediatr Res 53, 172 (2003). https://doi.org/10.1203/00006450-200301000-00112
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DOI: https://doi.org/10.1203/00006450-200301000-00112