Egger J, Stolla A, McEwen L M
Universitätskinderklinik, München, Germany.
Lancet. 1992 May 9;339(8802):1150-3. doi: 10.1016/0140-6736(92)90742-l.
Food intolerance seems to be an important cause of the hyperkinetic syndrome, but restricted diets are expensive, socially disruptive, and often nutritionally inadequate. Enzyme-potentiated desensitisation (EPD) may overcome some of these difficulties. EPD was tested in a double-blind placebo-controlled trial among 40 children with food-induced hyperkinetic behaviour disorder. A total of 185 children with established hyperkinetic syndrome underwent oligoantigenic dietary treatment for four weeks. 116 whose behaviour responded had provoking foods identified by sequential reintroduction. Foods that reproducibly provoked overactivity were avoided. 40 patients who were then invited to take part in the hyposensitisation trial were randomly assigned to treated and control groups. Treated patients received three doses of EPD (beta-glucuronidase and small quantities of food antigens) intradermally at two-monthly intervals. Controls received buffer only. Thereafter, patients were allowed to eat known provoking foods. Of 20 patients who received active treatment, 16 became tolerant towards provoking foods compared with 4 of 20 who received placebo (p less than 0.001). Our results show that EPD permits children with food-induced hyperkinetic syndrome to eat foods that had previously been identified as responsible for their symptoms. These results also support the notion that food allergy is a possible mechanism of the hyperkinetic syndrome.
食物不耐受似乎是多动综合征的一个重要病因，但限制饮食成本高昂、会扰乱社交，而且往往营养不足。酶增强脱敏疗法（EPD）或许能克服其中一些困难。在一项双盲安慰剂对照试验中，对40名患有食物诱发多动行为障碍的儿童进行了EPD测试。共有185名确诊为多动综合征的儿童接受了低抗原饮食治疗四周。116名行为有反应的儿童通过逐次重新引入食物确定了诱发食物。避免食用会反复引发多动的食物。随后，邀请40名患者参加脱敏试验，将他们随机分为治疗组和对照组。治疗组患者每隔两个月接受三次皮内注射EPD（β-葡萄糖醛酸酶和少量食物抗原）。对照组仅接受缓冲液。此后，允许患者食用已知的诱发食物。接受积极治疗的20名患者中，16名对诱发食物产生了耐受性，而接受安慰剂的20名患者中只有4名产生耐受性（p<0.001）。我们的结果表明，EPD使患有食物诱发多动综合征的儿童能够食用之前被确定为导致其症状的食物。这些结果也支持了食物过敏是多动综合征一种可能机制的观点。
