Moneret-Vautrin D A, Rance F, Kanny G, Olsewski A, Gueant J L, Dutau G, Guerin L
Medical department D, Internal Medicine, Clinical and Allergology, Hôpital Central, Nancy, France.
Clin Exp Allergy. 1998 Sep;28(9):1113-9. doi: 10.1046/j.1365-2222.1998.00370.x.
The increase in frequency of peanut allergy and fatal cases have been reported.
The objective of this study is to document the severity of food allergy to peanuts by evaluating the reactive dose of peanuts and to search for the role of peanut oil.
This study is carried out on the basis of 142 observations collected according to the same diagnostic methodology in two allergy centres in France. Skin-prick-tests were performed with peanut powder, peanut oil and peanut oil proteinic extract. Labial provocation tests were performed on 121 patients. The reactive dose of peanuts and the role of peanut oil were determined by standardized oral provocation tests in 50 and 62 patients respectively. The data are computerized and the data bank includes 509 food allergic patients.
Allergy to peanuts represents 28% of food allergies and occurs under 1 year of age in 46% of cases, under 15 years of age in 93%. The clinical features were atopic dermatitis (40%), angioedema (37%), asthma (14%), anaphylactic shock (6%) and digestive symptoms (1.4%). The specific IgE were class 3 or higher in 80% of cases. The total reactive dose was less than 100 mg in 25% of cases, from 100 mg to 1 g in 62.5%. All patients reacted to a dose of less than 7.1 g. The threshold of peanut reactivity was lower than the threshold of egg reactivity. An allergy to peanut oil was demonstrated in 14 patients.
The severity of peanut allergy and the early onset of the occurrence of this allergy is documented. The role of residual allergenic proteins in peanut oil is established by positive skin-prick tests to proteic extracts from peanut oil and by double-blind placebo-controlled challenges to peanut oil. The increased consumption of allergens in the form of peanut oil and fats can contribute to the occurrence or persistence of symptoms and may be suspected to increase the risk of sensitisation.
已有报道称花生过敏的发生率及致死病例有所增加。
本研究的目的是通过评估花生的反应剂量来记录对花生食物过敏的严重程度，并探寻花生油的作用。
本研究基于法国两个过敏中心按照相同诊断方法收集的142例观察病例开展。用花生粉、花生油及花生油蛋白提取物进行皮肤点刺试验。对121例患者进行唇黏膜激发试验。分别通过标准化口服激发试验在50例和62例患者中确定花生的反应剂量及花生油的作用。数据进行了计算机处理，数据库包含509例食物过敏患者。
花生过敏占食物过敏的28%，46%的病例在1岁以下发病，93%在15岁以下发病。临床特征为特应性皮炎（40%）、血管性水肿（37%）、哮喘（14%）、过敏性休克（6%）及消化道症状（1.4%）。80%的病例特异性IgE为3级或更高。25%的病例总反应剂量小于100mg，62.5%在100mg至1g之间。所有患者对小于7.1g的剂量均有反应。花生反应阈值低于鸡蛋反应阈值。14例患者证实对花生油过敏。
记录了花生过敏的严重程度及该过敏发病的早期情况。通过对花生油蛋白提取物皮肤点刺试验阳性及对花生油双盲安慰剂对照激发试验，证实了花生油中残留致敏蛋白的作用。以花生油和脂肪形式摄入的过敏原增加可能导致症状的发生或持续，并可能被怀疑会增加致敏风险。
