Search

A nine-year-old egg allergic child developed anaphylaxis after ingesting the lysozyme-containing over-the-counter-drug Lysopaine®. He complained of a sore throat without fever or cough. His mother administered him one sublingual tablet of the over-the-counter drug Lysopaine®, containing 20 mg lysozyme hydrochloride. A few minutes after intake of the drug, he developed anaphylaxis and received 300 mg intramuscular epinephrine. HE was not exposed to other allergens. The responsibility of lysozyme was confirmed by positive skin prick tests for Lysopaïne® and the presence of specific IgE against lysozyme. When giving this treatment to her son, his mother had no idea that it could contain egg protein and she did not perceive lysozyme as an allergenic protein. However, the box mentioned the presence of lysozyme and also specified “contains lysozyme extracted from egg”. Lysozyme, a minor egg allergen, may induce anaphylaxis in egg-allergic patients. Lysozyme can be found in many commonly consumed industrial food and drug products and its labelling may be misleading. Our observation highlights the importance of properly educating allergic patients to recognize allergens, even minor ones.

Background Food Protein-Induced Enterocolitis Syndrome (FPIES) is considered to be a non-IgE mediated food allergy. However, its pathogenesis remains poorly understood and biomarkers are lacking. We aimed to perform in-depth characterization of humoral and cellular immune responses in children with cow’s milk (CM)-FPIES and investigated whether there is a FPIES metabolomic signature. Methods Children with CM-FPIES and control subjects with an IgE-mediated CM allergy (IgE-CMA), both avoiding CM, were recruited on the day of an oral food challenge. Blood samples were collected before the challenge. Total and specific levels of IgE, IgG1-4, IgA, IgM and IgD to various whey and casein allergens and to their gastroduodenal digestion products were measured in plasma, using plasma from CM-tolerant peanut allergic patients (IgE-PA, not avoiding CM) as additional controls. Cytokine secretion and cellular proliferation were analyzed after stimulation of PBMC with different CM allergens. Metabolomic profiles were obtained for plasma samples using liquid chromatography coupled to high-resolution mass spectrometry. Results Nine children with CM-FPIES and 12 control subjects (6 IgE-CMA and 6 IgE-PA) were included. In children with CM-FPIES, total Ig concentrations were lower than in control subjects, specific Ig against CM components were weak to undetectable, and no specific IgE against CM digestion products were detected. Moreover, in CM-FPIES patients, we did not find any Th cell proliferation or associated cytokine secretion after allergen reactivation, whereas such responses were clearly found in children with IgE-CMA. Plasma metabolic profiles were different between CM allergic patients, with significantly lower concentrations of various fatty acids and higher concentrations of primary metabolites such as amino acids in CM-FPIES compared to IgE-CMA patients. Conclusions In CM-FPIES, both humoral and cellular specific immune responses are weak or absent, and this is not related to CM avoidance. A metabolomic signature was identified in patients with CM-FPIES that may be useful for the diagnosis and management of this disease. Electronic supplementary material The online version of this article (10.1186/s13601-018-0224-9) contains supplementary material, which is available to authorized users.