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可溶性黏附分子在丙种球蛋白无反应型川崎病中的表达
引用本文:刘凡,丁艳,尹薇. 可溶性黏附分子在丙种球蛋白无反应型川崎病中的表达[J]. 中国当代儿科杂志, 2013, 15(12): 1109-1112. DOI: 10.7499/j.issn.1008-8830.2013.12.018
作者姓名:刘凡  丁艳  尹薇
作者单位:刘凡, 丁艳, 尹薇
摘    要:
目的 探讨可溶性细胞间黏附分子-1(sICAM-1)在静脉注射丙种球蛋白(IVIG)无反应型川崎病(KD)患儿中表达的特点和意义。方法 选取使用IVIG治疗的KD患儿271例,其中IVIG敏感型252例,IVIG无反应型19例;发生冠脉扩张的患儿78例;同年龄健康对照组36例。ELISA法检测血浆sICAM-1水平,同时实验室检测全血WBC、中性粒细胞、CRP、血清谷草转氨酶、血钠和血钾水平。结果 IVIG治疗前,敏感型及无反应型患儿sICAM-1水平均明显高于对照组(P<0.05),且无反应型患儿sICAM-1水平亦高于敏感型患儿(P<0.05);IVIG治疗后24~48 h,无反应型患儿sICAM-1水平高于敏感型患儿(P<0.05);IVIG治疗前,IVIG敏感合并冠脉扩张患儿中sICAM-1水平明显高于IVIG敏感合并无冠脉扩张患儿(P<0.05),IVIG无反应合并冠脉扩张患儿sICAM-1水平亦明显高于IVIG无反应合并无冠脉扩张患儿(P<0.05);无反应型患儿sICAM-1水平与治疗前后WBC水平变化均呈正相关(分别r=0.7562、0.8435,均P<0.01),与治疗后CRP水平变化亦呈正相关(r=0.8936,P<0.01)。结论 高水平的sICAM-1表达可望作为预测KD患儿对IVIG反应情况及发生冠脉扩张的一项危险因素。

关 键 词:川崎病  静脉注射丙种球蛋白无反应  可溶性细胞间黏附分子-1  儿童  
收稿时间:2013-06-30
修稿时间:2013-07-17

Expression of sICAM-1 in children with intravenous immunoglobulin-resistant Kawasaki disease
LIU Fan,DING Yan,YIN Wei. Expression of sICAM-1 in children with intravenous immunoglobulin-resistant Kawasaki disease[J]. Chinese journal of contemporary pediatrics, 2013, 15(12): 1109-1112. DOI: 10.7499/j.issn.1008-8830.2013.12.018
Authors:LIU Fan  DING Yan  YIN Wei
Affiliation:LIU Fan, DING Yan, YIN Wei
Abstract:

Objective To investigate the expression of soluble intercellular adhesion molecule-1 (sICAM-1) and itd significance in children with intravenous immunoglobulin (IVIG)-resistant Kawasaki disease (KD). Methods A total of 271 children with KD who received IVIG treatment (including 252 IVIG-sensitive cases and 19 IVIG-resistant cases) were selected in the study; 78 of the 271 children had coronary artery dilation. Thirty-six age-matched healthy children were selected as the control group. Plasma sICAM-1 levels were measured using enzyme-linked immunosorbent assay. White blood cell count (WBC), neutrophil count, C-relative protein (CRP), aspartate aminotransferase(AST), serum sodium, and serum potassium were measured by laboratory tests. Results Before IVIG treatment, the IVIG-sensitive cases and IVIG-resistant cases had significantly higher sICAM-1 levels than the control group (P<0.05), and the IVIG-resistant cases had significantly higher sICAM-1 levels than the IVIG-sensitive cases (P<0.05). After 24-48 hours of IVIG treatment, the IVIG-resistant cases had significantly higher sICAM-1 levels than the IVIG-sensitive cases (P<0.05). Before IVIG treatment, among the IVIG-sensitive cases, the sICAM-1 level was significantly higher in those with coronary artery dilation than in those without coronary artery dilation (P<0.05); among the IVIG-resistant cases, the sICAM-1 level was significantly higher in those with coronary artery dilation than in those without coronary artery dilation (P<0.05). In the IVIG-resistant cases, sICAM-1 level was positively correlated with WBC (before and after treatment) (r=0.7562, P<0.01; r=0.8435, P<0.01) and CRP (after treatment) (r=0.8936, P<0.01). Conclusions High sICAM-1 level may be used as a risk factor for resistance to IVIG and coronary artery dilation in children with KD.

Keywords:

Kawasaki disease|Resistance to intravenous immunoglobulin|Soluble intercellular adhesion molecule-1|Child

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