Retrospective definition of reaction risk in Italian children with peanut, hazelnut and walnut allergy through component-resolved diagnosis

Background: Serum IgE evaluation of peanut, hazelnut and walnut allergens through the use of component-resolved diagnosis (CRD) can be more accurate than IgE against whole food to associate with severe or mild reactions. Objectives: The aim of the study was to retrospectively define the level of reaction risk in children with peanut, hazelnut and walnut sensitization through the use of CRD. Methods: 34 patients [n = 22 males, 65%; median age eight years, interquartile range (IQR) 5.0-11.0 years] with a reported history of reactions to peanut and/or hazelnut and/or walnut had their serum analyzed for specific IgE (s-IgE) by ImmunoCAP(R) and ISAC(R) microarray technique. Results: In children with previous reactions to peanut, the positivity of Arah1 and Arah2 s-IgE was associated with a history of anaphylaxis to such food, while the positivity of Arah8 s-IgE were associated with mild reactions. Regarding hazelnut, the presence of positive Cora9 and, particularly, Cora14 s-IgE was associated with a history of anaphylaxis, while positive Cora1.0401 s-IgE were associated with mild reactions. Concerning walnut, the presence of positive Jug r 1, Jug r 2, Jug r 3 s-IgE was associated with a history of anaphylaxis to such food. ImmmunoCAP® proved to be more useful in retrospectively defining the risk of hazelnut anaphylaxis, because of the possibility of measuring Cor a14 s-IgE. Conclusions: Our data show that the use of CRD in patients with allergy to peanut, hazelnut and walnut could allow for greater accuracy in retrospectively defining the risk of anaphylactic reaction to such foods

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Awareness of allergic enterocolitis among primary-care paediatricians: A web-based pilot survey

BACKGROUND: Allergic enterocolitis, also known as food protein-induced enterocolitis syndrome (FPIES), is an increasingly reported and potentially severe non-IgE mediated food allergy of the first years of life, which is often misdiagnosed due to its non-specific presenting symptoms and lack of diagnostic guidelines. OBJECTIVE: We sought to determine the knowledge of clinical, diagnostic and therapeutic features of FPIES among Italian primary-care paediatricians. METHODS: A 16-question anonymous web-based survey was sent via email to randomly selected primary care paediatricians working in the north of Italy. RESULTS: There were 194 completed surveys (48.5% response rate). Among respondents, 12.4% declared full understanding of FPIES, 49% limited knowledge, 31.4% had simply heard about FPIES and 7.2% had never heard about it. When presented with clinical anecdotes, 54.1% recognised acute FPIES and 12.9% recognised all chronic FPIES, whereas 10.3% misdiagnosed FPIES as allergic proctocolitis or infantile colic. To diagnose FPIES 55.7% declared to need negative skin prick test or specific-IgE to the trigger food, whereas 56.7% considered necessary a confirmatory oral challenge. Epinephrine was considered the mainstay in treating acute FPIES by 25.8% of respondents. Only 59.8% referred out to an allergist for the long-term reintroduction of the culprit food. Overall, 20.1% reported to care children with FPIES in their practice, with cow's milk formula and fish being the most common triggers; the diagnosis was self-made by the participant in 38.5% of these cases and by an allergist in 48.7%. CONCLUSION: There is a need for promoting awareness of FPIES to minimise delay in diagnosis and unnecessary diagnostic and therapeutic interventions

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Timing of introduction of solid food and risk of allergic disease development: Understanding the evidence

Strategies to prevent or reduce the risk of allergic diseases are needed. The time of exclusive breastfeeding and introduction of solid foods is a key factor that may influence the development of allergy. For this reason, the aim of this review was to examine the association between exposure to solid foods in the infant's diet and the development of allergic diseases in children. Classical prophylactic feeding guidelines recommended a delayed introduction of solids for the prevention of atopic diseases. Is it really true that a delayed introduction of solids (after the 4th or 6th month) is protective against the development of eczema, asthma, allergic rhinitis and food or inhalant sensitisation?. In recent years, many authors have found that there is no statistically significant association between delayed introduction of solids and protection for the development of allergic diseases. Furthermore, late introduction of solid foods could be associated with increased risk of allergic sensitisation to foods, inhalant allergens and celiac disease in children. Tolerance may be driven by the contact of the mucosal immune system with the allergen at the right time of life; the protective effects seem to be enhanced by the practice of the breastfeeding at the same time when weaning is started. Therefore, recent guidelines propose a “window” approach for weaning practice starting at the 17th week and introducing almost all foods within the 27th week of life to reduce the risk of chronic diseases such as allergic ones and the celiac disease. Guidelines emphasize the role of breastfeeding during the weaning practice (AU)

Neonatal sepsis and later development of atopy

Background: The role of infections on the development of atopy is still widely debated. We aimed to evaluate the effects of neonatal severe sepsis and consequent antibiotic treatment on the development of atopy and allergic diseases. Material and methods: A retrospective enrolment at school age of children with a clear history of neonatal sepsis (NS) was performed from registers of neonatal intensive care units. A normal control was assigned to each patient with sepsis. Thirty six cases with sepsis (18 males, 18 females) and 36 controls (21 males, 15 females) were selected (8.5±3.6 yrs). Physical examination and lung function evaluation were performed. Atopic status was verified by blood eosinophil count, total IgE serum level and skin prick tests (SPT). Results: SPT positivity for at least one allergen was present in 30% of subjects in both groups. No difference for all investigated parameters between groups and no influence by other factors such as familiarity or gender was observed. No correlation was associated to NS history. Conclusions: Neonatal sepsis, even if clinically severe and dramatic, could represent an event too limited and really precocious in life to influence the development of immune response. Furthermore, other factors, besides infections, may influence the atopic future of newborns (AU)

Bioimpedance monitoring of airway inflammation in asthmatic allergic children

Background: Asthma in childhood is characterized by chronic inflammation. Measurement of bioimpedance (BI) is a non-invasive way of detecting airway inflammation. The aim was to compare BI with exhaled nitric oxide (eNO) and lung function evaluations in asthmatic allergic children while not exposed to offending allergens. Methods: 22 asthmatic children allergic to house dust mites have been enrolled while residents at high altitude in an environment free of house dust mites. They were evaluated at T0 after allergen exposure at home, at T1 and at T2 after 1 and 4 months of allergen avoidance, respectively. Results: eNO decreased from 32.21 ± 5.70 ppb at T0 to 21.92 ± 4.36 ppb at T1, after one month at high altitude (p = 0.038), without a further decrease at T2. Data in electrical activity showed a significant decrease in conductivity of lower airways between T0 (48.53 ± 3.53 A) and T1 (42.08 ± 3.47 A) (p = 0.023). B parameter (difference between conductivity of lower respiratory tract and average yield) showed significant decrease from T0 (20.75 ± 2.64 A), and T1 (12.84 ± 2.52 A) (p < 0.01), but no further decrease at T2. No difference in lung function parameters was observed. Conclusion: Allergen avoidance regimen modifies inflammatory parameters in allergic asthmatics. Evaluation of extracellular bioelectrical conductivity seems to represent a promising non-invasive method to assess airway inflammation (AU)

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