가와사끼병에서 가용성 ELAM - 1 에 관한 연구 = Serum soluble endothelial leukocyte adhesion molecule - 1 level in Kawasaki disease

다국어 초록 (Multilingual Abstract)

Kawasaki disease is an acute systemic disease with clinical manifestions of vasculitis. There have been many studies concerning the etiology and pathogenesis of the disease. But they have not yet been clarified. Rececntly among various surface antigens expressed on the cell membrane during the activation of the vascular endothelial cells, the intercellular adhesion molecules which bind with the peripheral blood leukocytes have been studied a great deal. Especially the endothelial leukocyte adhesion molucule-l (ELAM-1), which is expressed only on the vascular endothelial cells, is gathering interests of many researchers. The ELAM-1, which can be detected in the blood as a soluble antigen shedded from the cell membrane, could be used as an index of severity of the vasculitis in inflammatory diseases. In this study the serum soluble ELAM-1 levels along with C-reactive protein(CRP), and tumor necrosis factor-α (TNF-α) levels have been determined in the patients with Kawasaki disease to see the relationship with the degree of vasculitis. The study subjects were 24 patients with Kawasaki disease, 10 with Henoch-Schonlein purpura, and 18 with Behcet’s disease who were admitted to the Department of Pediatrics, Severanc Hospital between September 1992 and June 1993. Ten children who were admitted for elective surgery consisted of the negative control group. The serum samples were obtained during the acute and subacute stages, stored frozen at-70ºC, and thawed at room temperature just before the measurement. The serum soluble ELAM-1 levels were measured by the sandwich ELISA method (Bender Med Systems), and TNF- α levels by the sandwich ELISA method(R&D System). CRP was measured by the fluorescence polorization immunoassay method. The serum soluble ELAM-1 level rapidly rose up to 27.5ng/ml during the acute stage and fell to 16.2ng/ml during the subacute stage. Similary TNF-α level increased to 44.1pg/ml during the acute stage and significantly decreased to 24.0pg/ml during the subacute stage. In the patients with Henoch-Schonlein purpura, the serum soluble ELAM-1 level was elevated to 12.9ng/ml, which was higher as compared to the normal elvel(less than 6ng/ml), but not as high as that in the patients with Kawasaki disease. For Behcet’s disease it was 5.5ng/ml; that is not at all higher than the normal level. There was a linear relationship between the serum soluble ELAM-1 levels of the Kawasaki patients and the serum TNF-α. However, the serum CRP or ESR did not show any direct relationship with the serum soluble ELAM-1 levels. As the results suggest, the serum soluble ELAM-1 levels increase in proportion with the degree of vasculitis. And whether the ELAM-1, which is expressed on the cell surface of the vascular endothelium, is related to the pathogenesis of Kawasaki disease must further be studied.