Asian Pacific journal of allergy and immunology · 2025
Children with wheat anaphylaxis and with low wheat specific IgE have a different IgE immunoblot pattern than those with high wheat specific IgE.
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Rutrakool Nuntanut, Piboonpocanun Surapon, Wangthan Unchalee, Srisuwatchari Witchaya, Thongngarm Torpong, Jirapongsananuruk Orathai, Visitsunthorn Nualanong, Vichyanond Pakit, Pacharn Punchama
Аннотация
BACKGROUND: Children with wheat anaphylaxis can present with a wide range of wheat-specific IgE (sIgE).
OBJECTIVE: To identify differences in clinical features and predominant wheat allergens sensitized by these patients.
METHODS: Children with history of wheat anaphylaxis were recruited. Skin prick test (SPT) to wheat, sIgE to wheat, omega-5 gliadin (ω5G), lipid transfer protein (LTP) were investigated. Profiles of IgE-bound wheat allergens were studied to identify predominant wheat allergens.
RESULTS: Twenty-nine children (17 males) aged 1-18 years were enrolled. Sixteen patients (55.2%) had wheat-sIgE > 100 kUA/L (WAhi) and 13 patients (44.8%) had wheat-sIgE < 34 kUA/L (WAlo). The median of peak wheat-sIgE in WAhi and WAlo were 340.5 kUA/L (IQR 184.3, 564.5) and 12.2 kUA/L (IQR 1.4, 41.3), respectively. Oral food challenge test (OFC) was carried out in 12 of 13 patients in the WAlo group, all of which had positive results. Eight of these 12 patients developed anaphylaxis during OFC despite having wheat-sIgE less than 10 kUA/L. There were no differences in clinical characteristics and atopic history between WAhi vs. WAlo. Medium to low molecular weight gliadin (< 40 kDa) and glutenin (< 60 kDa) were commonly recognized by patients with WAhi. IgE immunoblot pattern among the WAlo group was more widely dispersed than those with WAhi.
CONCLUSIONS: Wheat anaphylaxis can occur in patients with low wheat-sIgE. Predominant wheat allergens recognized by patients with WAlo were different than those with WAhi. Such difference could be responsible for anaphylaxis at even low levels of wheat-sIgE.
OBJECTIVE: To identify differences in clinical features and predominant wheat allergens sensitized by these patients.
METHODS: Children with history of wheat anaphylaxis were recruited. Skin prick test (SPT) to wheat, sIgE to wheat, omega-5 gliadin (ω5G), lipid transfer protein (LTP) were investigated. Profiles of IgE-bound wheat allergens were studied to identify predominant wheat allergens.
RESULTS: Twenty-nine children (17 males) aged 1-18 years were enrolled. Sixteen patients (55.2%) had wheat-sIgE > 100 kUA/L (WAhi) and 13 patients (44.8%) had wheat-sIgE < 34 kUA/L (WAlo). The median of peak wheat-sIgE in WAhi and WAlo were 340.5 kUA/L (IQR 184.3, 564.5) and 12.2 kUA/L (IQR 1.4, 41.3), respectively. Oral food challenge test (OFC) was carried out in 12 of 13 patients in the WAlo group, all of which had positive results. Eight of these 12 patients developed anaphylaxis during OFC despite having wheat-sIgE less than 10 kUA/L. There were no differences in clinical characteristics and atopic history between WAhi vs. WAlo. Medium to low molecular weight gliadin (< 40 kDa) and glutenin (< 60 kDa) were commonly recognized by patients with WAhi. IgE immunoblot pattern among the WAlo group was more widely dispersed than those with WAhi.
CONCLUSIONS: Wheat anaphylaxis can occur in patients with low wheat-sIgE. Predominant wheat allergens recognized by patients with WAlo were different than those with WAhi. Such difference could be responsible for anaphylaxis at even low levels of wheat-sIgE.