Summary Background.
Allergy to kiwi is currently one of the most common causes of food allergy, and offers a clear example of the effects of the introduction of a new food in the food chain. In recent European epidemiological studies it was shown to be among the top ten sources of allergy. It is often associated with sensitization to birch pollen with symptoms localized to the oral cavity (oral allergy syndrome, OAS). Some patients, however, experience systemic symptoms such as acute urticaria, angioedema, gastrointestinal and/or cardiovascular symptoms or anaphylaxis. 13 kiwi allergens were identified, 4 of which are available for specific IgE testing on the microarray test panel: 3 are kiwi specific components (Act d 1, Act d 2, Act d 5), and 1 is a cross-reactive protein, belonging to the PR-10 protein family (Act d 8). The aim of the study was to identify the allergenic sensitization profile in a group of pediatric patients with suspected allergy to kiwi, who showed symptoms, in almost all cases suggestive of severe allergy.
Methods.
Between January 2012 and December 2017 25 patients (aged 1–14 years; 19 Males/6 Females), presented specific IgE test requests for kiwi to the Allergology Laboratory of Udine. The symptoms most frequently associated with ingestion, or to mere contact with the fruit, were facial angioedema and acute urticaria, followed by OAS, gastrointestinal symptoms, rhinoconjunctivitis, respiratory symptoms, dermatitis and, in 6 patients, anaphylaxis. In all the sera, specific IgE to the whole extract and to the singular components were detected by using the ImmunoCAP and the ImmunoCAP ISAC assay, respectively (Thermo Fisher Diagnostics, Uppsala, Sweden).
Results.
All patients were positive for IgE to kiwi extract; the profile for molecular allergens, in 22 sera (88%) showed positivity for the major allergen Act d 1, in 4 (16%) for Act d 2, and in 2 (8%) for Act d 5. In 4 subjects multiple sensitizations (Act d1 + Act d 2 / or Act d 5) was shown. IgE anti-Act d 8 were detected in 3 cases, combined to anti-Act d1 presence. One child affected by OAS resulted positive to Bet v 1 (Birch PR-10), but not to Act d 8 (kiwi PR-10).
Conclusions.
In case of suspected kiwi allergy in the pediatric population, it is crucial to perform IgE tests using both the extractive allergen and the expanded molecular profile with the microarray test. The presence of IgE for one of the specific allergens, even if associated with positivity for PR-10, reinforces the diagnosis of risk of severe allergy and urges avoidance of the food. The study confirms that kiwi allergy in childhood is caused by primary IgE sensitization and that positivity for Act d 1 is an indicator and risk factor for severe allergy.