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All issues > Volume 50(12); 2007

Original Article
Korean J Pediatr. 2007;50(12):1241-1246. Published online December 15, 2007.
Influence of vascular endothelial growth factor (VEGF) and endostatin on coronary artery lesions in Kawasaki disease
Seon A SA Kim1, Bum Suk BS Jung1, Jong Seo JS Yoon1, Ji Whan JW Han1, Joon Sung JS Lee1
1Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea
Correspondence Ji Whan JW Han ,Email: han59@catholic.ac.kr
Abstract
Purpose
Recently, there has been several studies to clarify the pathogenesis of Kawasaki disease (KD) and the relations of VEGF and endostatin that act on vascular endothelial cells to the coronary artery complications. In this report, we measured serum levels of VEGF and endostatin in acute and subacute phases of KD to assess the change of these levels and the relations to the development of coronary artery lesions (CAL).
Methods
Twenty six patients were diagnosed and treated for KD between January, 2001 and July, 2005 at Kangnam St. Mary's Hospital, the Catholic University of Korea. They were divided into those with and without CAL. Serum levels of VEGF and endostatin were measured during acute and subacute phases and compared to those measured in healthy and disease control groups.
Results
Serum levels of VEGF were increased in KD but no differences were noted in KD with and without CAL. Serum levels of endostatin were decreased in the acute phase of KD, however they were recovered in the subacute phase of KD, regardless of CAL. The VEGF/endostatin ratio was increased in KD. KD without CAL showed a relative decrease in this ratio during the subacute phase. Significant positive correlations were found between serum VEGF and WBC count, VEGF and ESR, VEGF/endostatin ratio and ESR in the acute phase of KD.
Conclusion
Analysis of factors influencing the vascular endothelium such as VEGF and endostatin will help to clarify the etiology of KD and the pathogenesis of CAL.

Keywords :Kawasaki disease, Vascular endothelial growth factor, Endostatin

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