Protein‐losing enteropathy and erythema caused by egg allergy in a breast‐fed infant

A 4‐month‐old breast‐fed girl presented with poor weight gain, and had edema and repeated erythema from 5 months of age. The diagnosis of protein‐losing enteropathy (PLE) was confirmed on ^99mTc‐labeled human serum albumin scintigraphy. Specific IgE radioallergosorbent test was class 3 for egg white, class 2 for egg yolk, and negative for other foods. Elimination of egg from the mother's diet and oral epinastine hydrochloride treatment and sodium cromolyn improved hypoalbuminemia, hypogammaglobulinemia, and erythema. PLE and erythema coincident in a breast‐fed infant suggests that IgE‐mediated allergy may play a leading role in some cases of PLE due to food allergy in infants.     

IgE介导的食物过敏诊断程序及临床评价

目的 对IgE介导的食物过敏的诊断流程进行临床评价。探讨高效的食物过敏诊断程序。方法 0～6岁患儿88例,以支气管哮喘、过敏性鼻炎、特应性皮炎以及消化道症状为主要临床表现,进行食物过敏原皮肤点刺试验（skin prick test,SPT）,皮肤试验阳性者检测血清特异性IgE（sIgE）、sIgE阳性者进一步进行双盲安慰剂食物激发试验（double-blind placebo-control food challenge,DBPCFC）证实诊断。sIsE阴性者通过DBPCFC建立或排除诊断。结果 88例患儿中SPT（＋）者25例。其中SPT（＋）sIgE（＋）者16例,SPT（＋）sIsE（-）者9例;前者经DBPCFC进一步证实为食物过敏的有14例;后者通过DBPCFC建立诊断的3例。排除诊断的6例,根据SPT（＋）sIgE（＋）或SPT（＋）sIsE（-）诊断食物过敏的阳性预计值为87．5％．阴性预计值为77．8％。结论 皮肤点刺试验结合sIgE检测有较高的食物过敏确诊率,当前两者不一致时,需要通过DBPCFC建立诊断。     

Peanut seed storage proteins are responsible for clinical reactivity in Spanish peanut‐allergic children

Background: Seed storage proteins (SSP; Ara h 1, Ara h 2, Ara h 3) have been shown to be major peanut allergens, although recently, peanut lipid transfer protein has been reported to be an important allergen in the Mediterranean area. We sought to investigate the sensitization pattern to peanut SSP and vegetable pan‐allergens in a group of peanut‐allergic children compared with a peanut‐tolerant group. Methods: One hundred and twenty‐three children who presented with food allergy were included in the study. Tolerance to peanut ingestion was assessed. Specific IgE was determined by ImmunoCAP, and microarray ISAC was performed. Sensitization frequencies and levels of specific IgE were compared between groups. Results: Fifty‐five of 123 children presented symptoms upon contact or ingestion. Frequency of sensitization to Ara h 1, Ara h 2, and Ara h 3 was 60.0%, 72.7%, and 43.6%, respectively, in the group of allergic children vs. 7.4%, 1.5%, and 7.4% in the group of tolerant children. Levels of specific IgE against Ara h 1, Ara h 2, and Ara h 3 were significantly higher in the allergic group (p < 0.001). The frequency of sensitization and the levels of specific IgE against Cor a 8 (36.4% vs. 16.2%) were significantly higher in the allergic children, whereas no significant differences were found for Pru p 3. No differences were seen for other pan‐allergens. Patients sensitized to SSP, regardless of sensitization to nsLTP, were allergic rather than tolerant. Conclusion: In our population, peanut‐allergic children were mainly sensitive to SSP. A few patients were also sensitive to some nsLTPs. No differences were shown in other pan‐allergens.     

Treating IgE‐mediated diseases via targeting IgE‐expressing B cells using an anti‐CεmX antibody

Targeting the IgE pathway is a clinically validated strategy for treating IgE‐mediated diseases. Omalizumab, an anti‐IgE antibody, which binds to free IgE and prevents the binding of IgE to FcεRI on mast cells and basophils has been approved for severe persistent allergic asthma and chronic spontaneous (idiopathic) urticaria. The therapeutic efficacy of anti‐IgE has also been reported in allergic rhinitis, allergic bronchopulmonary aspergillosis, latex allergy, atopic dermatitis, allergic urticaria, anaphylaxis, and others. Anti‐CεmX, which binds to membrane‐bound IgE (mIgE) on IgE‐switched B cells, lyses mIgE‐expressing B lymphoblasts and prevents the allergen‐induced generation of IgE‐producing plasma cells, offers an alternative mechanism of intervening with the IgE inflammatory pathway. Because anti‐CεmX does not bind to free IgE, it can modulate the IgE pathway regardless of the serum IgE levels in treated patients. These unique pharmacologic mechanisms potentially enable anti‐CεmX to provide different clinical utilities from anti‐IgE and serve as a therapeutic and a prophylactic in some IgE‐mediated diseases, which are not adequately treated with current medicine.