食物过敏患儿血清特异性IgG抗体、sIL-2R检测分析

目的探讨食物过敏患儿血清食物特异性IgG(sIgG)抗体、可溶性白介素-2受体(sIL-2R)水平的变化及二者的关系。方法将48例慢性、迁延性腹泻患儿,经食物回避-激发试验确定为食物过敏患儿作为观察组,另选取24例性别、年龄相匹配的健康小儿作为对照组,采用ELISA法检测小儿血清中14种食物sIgG抗体浓度及sIL-2R水平。结果观察组食物过敏原IgG检出阳性率为83.3%,对照组均在正常范围之内。观察组血清sIL-2R水平较对照组显著升高(P<0.05),观察组食物sIgG阳性组较阴性组显著升高(P<0.05)。腹泻患儿血清sIL-2R水平与牛奶lgIgG(sIgG抗体经对数转换后)水平成正相关(r=0.437,P<0.05);观察组食物sIgG阳性组sIL-2R水平分别与牛奶lgIgG、鸡蛋lgIgG成正相关(r分别为0.531,0.344,P<0.05)。结论食物过敏患儿血清sIL-2R的升高与部分食物sIgG抗体有相关性。血清sIL-2R水平增高,是检测非IgE介导的食物过敏的重要指标之一。

Objective To explore the changes and the relationship between serum food specific IgG（sIgG） antibodies and soluble Interleukin-2 receptor（sIL-2R） in infancy with food allergen. Methods Selected 48 infancy with persistent and chronic diarrhea for the observation group ,who were fed Artificial and identified food allergy after food evade - the provocation tes,and 24 normal children as control group, which are similar in gender and age. The mean of ELISA was adopted to test serum food sIgG antibodies and sIL-2R.Results The positive rate of serum food-specific IgG was 83.3% in infancy with persistent and chronic diarrhea, the control group are negative. The levels of sIL-2R in children with the observation group were significantly higher than those in young children with the control group （P〈0.05）;The sIL-2R levels in infancy with the observation positive group were significantly higher than those in children with the observation negative group （P〈0.05）; There were a positive correlation between the level of sIL-2R and cow＇s milk lgIgG （IgG antibody concentration has been transformed by the logarithmic）in young children with persistent and chronic diarrhea（r = 0.437,P〈0.05）.The level of sIL-2R,which is in the observation positive group, is a positive correlation with the corresponding milk lgIgG or egg LgIgG （r= 0.531,0.344, P〈0.05）;Conclusion Serum sIL-2R increased were correlated with some food allergy IgG in persistent and chronic diarrhea.Serum sIL-2R increased,which can be used as a indicator in infancy with food allergy that was non-IgE-mediated.