Measuring breakthrough exercise-induced bronchoconstriction in young asthmatic children using a jumping castle

abolished by preincubation with the monomer or dimer. This inhibition appeared to be antigen specific, as anti‐IgE-induced HR remained unchanged after preincubation with the monomer and dimer (25 and 21 ng histamine/mL, respectively). These results, in combination with those of the passive sensitization experiment, strongly indicate that serum factors in the patient’s blood, possibly IgE antibodies, may bind monovalent ethylene glycol. However, only repetitive presentation of this structure in the form of a polymer chain induces a biological response as demonstrated by a positive SPT and HR test result to PEGs. The patient’s anamnesis, clinical symptoms, and positive SPT results for PEG 3350, PEG 6000, Depo-Medrol, Balancid, and other PEG-containing products point to PEG allergy. Also, positive direct and passive HR tests, as well as the successful inhibition of PEG-induced basophil HR by monomer and dimer fractions of PEG and omalizumab, indicate an IgE-mediated mechanism. Nonetheless, in the absence of a commercially available specific IgE assay for PEG, the mechanism can only be limited to an unidentified serum factor. To our knowledge, this is the first time an IgE-mediated crosslinking mechanism has been made plausible by inhibition studies using monovalent haptens. We present a unique case of allergy to PEGs of varying molecular weights and exposure routes, with responses provoked by intramuscular (Depo-Medrol), per oral (Balancid), and possibly, intradermal administration (via tattooing). We recommend testing patients for PEG allergy in instances of repeated, idiopathic reactions to PEGcontaining substances. With increasing use of PEGs in both household and pharmaceutical products, as well as drug-delivery technology, 2 an increase in the incidence of allergy to these pol

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