Pediatric Allergy and Immunology最新文献

Background: Several major sensitization profiles have been described in children with asthma, but it remains unclear how these profiles relate to asthma phenotypes. The aim of this study was to determine allergenic sensitization profiles in a megacity cohort (SAMP).

Methods: This was a cross-sectional analysis performed from 2011 to 2015 including preschool and school-age children with severe and moderate asthma from the SAMP cohort. We performed ALEX multiplex array and carried out cluster analysis.

Results: Data from 367 children were analyzed: 224 of preschool age and 143 of school age, respectively 84 (38%) and 114 (80%) presented at least one allergic sensitization. At preschool age, three clusters were identified: Cluster 1, Few sensitizations to inhaled allergen molecular families and non-type 2 (T2) inflammation (n = 61); Cluster 2, Predominant sensitization to HDM molecular families (n = 16); Cluster 3, Severe asthma with multiple sensitizations to inhaled and food allergen molecular families (n = 7). At school age, five clusters were identified: Cluster 1, Few sensitizations to inhaled allergen molecular families and non-T2 inflammation (n = 43); Cluster 2, Predominant sensitization to HDM molecular families (n = 31); Cluster 3, Predominant sensitization to PR-10 protein family (n = 25); Cluster 4, Severe asthma with predominant sensitization to tropomyosin family (n = 11); Cluster 5, Severe asthma with multiple sensitizations to inhaled and food allergen molecular families (n = 4).

Conclusion: These results underline the heterogeneity of sensitization profiles in severe allergic childhood asthma. The most severe asthma phenotypes were associated with multiple sensitizations to both inhaled and food allergen molecular families as expected, and to the tropomyosin molecular family, a novel finding.

Allergic diseases including food allergy, atopic dermatitis, asthma, and allergic rhinitis are increasing. Nutritional intake may play a role in this increase. Systematic reviews indicate that intake of specific nutrients and foods does not prevent allergic diseases. The role of the overall diet as measured by dietary patterns (Diet diversity, Dietary inflammatory index, Mediterranean diet score, Healthy eating index, Maternal diet index, ultra-processed food dietary patterns, and others) have not been systematically reviewed. We aim to investigate the association between overall maternal dietary intake during pregnancy and offspring allergy outcomes. The following databases will be searched: PubMed, OVID Medline, Web of Science, and Embase. Studies with publication dates up to November 28, 2024, will be eligible. We will perform our last search on November 28, 2024. There will be no restrictions by geographical location but only studies published in English will be included. Risk of bias in the included studies will be assessed using the ROBINS-I Cochrane assessment tool. Data will be discussed and narratively, and studies that present comparable data will be used in meta-analyses with a random effects model. Data will be discussed and narratively, and studies that present comparable data will be used in meta-analyses with a random effects model. The results of this systematic review and meta-analysis will be published in a peer-reviewed journal. Systematic reviews provide methodology for objective evidence synthesis. The systematic review will provide useful information regarding the role of maternal dietary patterns during pregnancy and their association with offspring allergy outcomes.

The earliest respiratory function assessments, within or close to the neonatal period, consistently show correlations with lung function and with the development of asthma into adulthood. Measurements of lung function in infancy reflect the in utero period of lung development, and if early enough, show little influence of postnatal environmental exposures. Later in the preschool and school age periods, influences of the environment are superimposed on initial levels. Fetal exposures before birth such as maternal smoking during pregnancy, lead to reduced lung function and an increased risk of asthma in females particularly those with certain glutathione S-transferase genotypes. Lung function measurements later in the preschool period are also associated with development of asthma. Although lung function in preschoolers does help predict asthma in later life and these observations have increased our understanding of the physiology underlying asthma, the findings have not led to thewidespread use of lung function measurements being in preschoolers as clinical predictors of asthma due to the practicalities of testing in this age group.

Background: Hereditary angioedema (HAE) in children has specific features and requires multidisciplinary management.

Methods: We performed a literature search and underwent in-depth discussions to provide practical tools for physicians.

Results: HAE is a rare, life-threatening genetic disorder. Its epidemiology is poorly documented in children. Clinical manifestations usually appear during childhood or early adolescence. Classical signs, often preceded by prodromal symptoms, include transient, localized, non-pitting, non-pruritic swelling of deep dermal/subcutaneous or mucosal/submucosal tissues, leading to oedema of the extremities, face, lips, tongue, trunk and genitals, recurring gastrointestinal symptoms and laryngeal edema possibly causing asphyxiation and death. Diagnosis is often delayed due to low awareness in the medical community, and particularly challenging in case of isolated abdominal crises or atypical presentation and in neonates or infants. It relies on biological tests (measurement of serum/plasma levels of C1INH function, C1INH protein, and C4), genetic testing in selected cases, and imaging for differential diagnosis of acute abdominal crises. Main differential diagnosis for peripheral oedema is mast cell-mediated oedema that accounts for 95% of angioedema in clinical practice. Quality of life can be significantly impaired. Disease management includes treatment of attacks, short-term and long-term prophylaxis, psychological support, avoidance of triggers, patients' and parents' education and coordination of all stakeholders, ideally within a specialized healthcare network. New plasma kallikrein inhibitors, namely lanadelumab (subcutaneous route) and berotralstat (oral route) have facilitated long-term prophylaxis thanks to improved usability.

Conclusion: Diagnostic and treatment of HAE are particularly challenging in children and require specific management by multiple stakeholders.

Background: Wheezing is common in early life, but most children stop wheezing by school age. However, the prediction of course of wheezing through childhood is difficult.

Objective: To investigate whether urinary EPX (a marker of eosinophil activation) in children at age 3 years may be useful for the prediction of wheeze persistence and future asthma diagnosis.

Methods: U-EPX was measured at age 3 years (radioimmunoassay) in 906 participants in the population-based birth cohort. Children attended follow-ups to age 16 years. We investigate the discriminative ability of u-EPX and other factors in predicting asthma diagnosis at age 16 using receiver operating characteristic [ROC] curves.

Results: Of 613 children with follow-up information at age 16, 511 had data on u-EPX at age 3 and asthma diagnosis at age 16 years; of those; 133 (21.7%) had asthma. Based on longitudinal data, children were assigned to wheeze clusters: No wheeze (NWZ), early transient (ETW), late-onset (LOW), intermittent (INT) and persistent wheeze (PEW). U-EPX levels differed significantly between different wheeze clusters (p = .003), with clusters characterised with persistent symptoms having higher u-EPX. In the whole cohort, the best performing classification model for asthma diagnosis at age 16 years included sex, u-EPX, sensitisation and wheeze (area under the curve (AUC) = 0.82, 95% CI: 0.76-0.88). u-EPX and allergic sensitisation alone had similar predictive power (AUC [95%CI]: 0.64 [0.58-0.71] and 0.65 [0.60-0.71]). The best performing classification model for asthma prediction among children with doctor-confirmed wheeze in the first 3 years included child's u-EPX and sensitisation at age 3 years, sex, gestational age and maternal atopy (AUC: 0.76, 95%CI: 0.67-0.85).

Conclusions: Early-life u-EPX may be a useful non-invasive marker for asthma prediction in adolescence.