School of Translational Medicine, University of Manchester, NIHR Translational Research Facility in Respiratory Medicine, University Hospital of South Manchester NHS Foundation Trust, Manchester M23 9LT, United Kingdom.
J Allergy Clin Immunol. 2010 Jan;125(1):191-7.e1-13. doi: 10.1016/j.jaci.2009.10.008.
Not all peanut-sensitized children develop allergic reactions on exposure.
To establish by oral food challenge the proportion of children with clinical peanut allergy among those considered peanut-sensitized by using skin prick tests and/or IgE measurement, and to investigate whether component-resolved diagnostics using microarray could differentiate peanut allergy from tolerance.
Within a population-based birth cohort, we ascertained peanut sensitization by skin tests and IgE measurement at age 8 years. Among sensitized children, we determined peanut allergy versus tolerance by oral food challenges. We used open challenge among children consuming peanuts (n = 45); others underwent double-blind placebo-controlled challenge (n = 34). We compared sensitization profiles between children with peanut allergy and peanut-tolerant children by using a microarray with 12 pure components (major peanut and potentially cross-reactive components, including grass allergens).
Of 933 children, 110 (11.8%) were peanut-sensitized. Nineteen were not challenged (17 no consent). Twelve with a convincing history of reactions on exposure, IgE > or =15 kUa/L and/or skin test > or =8mm were considered allergic without challenge. Of the remaining 79 children who underwent challenge, 7 had > or =2 objective signs and were designated as having peanut allergy. We estimated the prevalence of clinical peanut allergy among sensitized subjects as 22.4% (95% CI, 14.8% to 32.3%). By using component-resolved diagnostics, we detected marked differences in the pattern of component recognition between children with peanut allergy (n = 29; group enriched with 12 children with allergy) and peanut-tolerant children (n = 52). The peanut component Ara h 2 was the most important predictor of clinical allergy.
The majority of children considered peanut-sensitized on the basis of standard tests do not have peanut allergy. Component-resolved diagnostics may facilitate the diagnosis of peanut allergy.
并非所有花生致敏的儿童在接触后都会出现过敏反应。
通过口服食物激发试验，确定在使用皮肤点刺试验和/或 IgE 测量被认为是花生致敏的儿童中，有临床意义的花生过敏的比例，并研究使用微阵列的成分分辨诊断是否可以将花生过敏与耐受区分开来。
在一项基于人群的出生队列中，我们在 8 岁时通过皮肤试验和 IgE 测量来确定花生致敏情况。在致敏儿童中，我们通过口服食物激发试验来确定花生过敏与耐受。对于食用花生的儿童（n=45），我们进行了开放性激发试验；对于其他儿童（n=34），我们进行了双盲安慰剂对照激发试验。我们使用含有 12 种纯成分（主要花生和潜在交叉反应成分，包括草过敏原有）的微阵列来比较花生过敏和花生耐受儿童的致敏谱。
在 933 名儿童中，有 110 名（11.8%）是花生致敏的。有 19 名儿童未接受挑战（17 名儿童不同意）。有 12 名儿童有明确的接触暴露后出现过敏反应、IgE≥15 kUa/L 和/或皮肤试验≥8mm 的病史，未进行激发试验即被认为是过敏。在其余 79 名接受激发试验的儿童中，有 7 名儿童出现≥2 项客观体征，被诊断为花生过敏。我们估计，在致敏儿童中，有临床意义的花生过敏的患病率为 22.4%（95%CI，14.8%至 32.3%）。通过成分分辨诊断，我们检测到花生过敏儿童（n=29；该组有 12 名过敏儿童）和花生耐受儿童（n=52）之间在成分识别模式上有显著差异。花生成分 Ara h 2 是预测临床过敏的最重要因素。
根据标准检测被认为是花生致敏的大多数儿童实际上并没有花生过敏。成分分辨诊断可能有助于花生过敏的诊断。
