Kristina Rueter

Background: Rates of anaphylaxis in early childhood are rising, yet there remains a paucity of data on age‐specific presentations and outcomes. While prompt treatment is essential, symptoms can differ from older children. Observation after stabilization is routinely used; however, no infant and toddler‐specific data guide the duration of monitoring. Identifying predictors of biphasic anaphylaxis could help guide observation times. Objective: To characterize symptoms of anaphylaxis in infants and toddlers, analyze predictors for biphasic anaphylaxis and get more insight into required observation times in this age group. Methods: Anaphylaxis cases aged 0–2 years presenting to a major Emergency Department (ED) were reviewed over two 5‐year‐periods. We analyzed clinical features, allergens, and management, comparing uniphasic and biphasic presentations. Results: Of 567,595 total ED presentations aged 0–16 years, 243 cases of 0–2‐year‐olds (infants/toddlers) presented with anaphylaxis (72/236,217 in 2003–2007; 171/331,378 in 2013–2017). Symptoms included urticaria (85.8%), angioedema (67.8%), wheeze/persistent cough (57.7%), vomiting (42.3%) and flushing (21.8%). Symptoms unique to infants/toddlers were pallor/hypotonia (33.5%) and persistent crying (13.8%). Biphasic anaphylaxis occurred in 4.6%, was exclusively food‐induced and more common among infants ( p = .048). Predictors for biphasic anaphylaxis were lower systolic blood pressure ( p = .011), pallor/hypotonia ( p = .046), use of fluids ( p < .001), and greater severity ( p = .014). Timeframe for recurrence of anaphylaxis was 70–330 min. Conclusion: Increased awareness of age‐specific symptoms is essential for timely recognition and optimal care of infant/young toddler anaphylaxis. Cardiovascular signs, fluid resuscitation, and reaction severity may help predict recurrent anaphylaxis in 0–2‐year‐olds and identify which patients need observation beyond 4 h versus those safe for earlier discharge. image

Background: The Australasian Society of Clinical Immunology and Allergy (ASCIA) Guideline: Infant Feeding for Food Allergy Prevention is an update of the 2016 ASCIA guideline. This updated guideline provides recommendations specifically in relation to infant feeding for food allergy prevention. Methods: A review of the guideline began in 2024, informed by a systematic evidence review process and using the Appraisal of Guidelines for Research & Evaluation II (AGREE II) framework. Where evidence was lacking, a formal Delphi process was used to develop recommendations based on expert consensus. An Expert Writing Group comprising representation from ASCIA, the National Allergy Council, Allergy & Anaphylaxis Australia the National Allergy Centre of Excellence and the Centre for Food Allergy Research was established. Key stakeholder meetings were held. Results: A systematic review of evidence resulted in 16 recommendations: eight based on published evidence; eight based on expert consensus. ASCIA recommends: In Australia and New Zealand, infants should be introduced to solid foods when they are showing signs of developmental readiness. This is usually around 6 months and not before 4 months of age. Soon after infants have started solid foods, well cooked egg and appropriate forms of peanut are included in the infant's diet. Other common food allergens included in the family diet should be offered to the infant. Once introduced, common food allergens should be offered around once a week. Breastfeeding is encouraged, with no maternal dietary modifications. Breastmilk substitutes based on hydrolysed milk protein, soy or other proteins are not recommended for allergy prevention. Mild perioral rashes which appear around food consumption (redness or contact urticaria with no other symptoms of allergy) may not be a sign of an allergic reaction, and the food should be offered again. Conclusion: Key changes from the 2016 ASCIA guideline include specific recommendations regarding the timing of peanut and egg introduction, alongside a recommendation regarding perioral rashes to support primary healthcare providers. These guidelines require ongoing review and updating as new evidence emerges.

Aim: The incidence of anaphylaxis is increasing globally in tandem with changing environmental and lifestyle factors. There is very limited data on very early childhood presentations. We aim to assess changes in rates, characteristics and management of infant anaphylaxis in a paediatric ED over a 15‐year period.Methods: We conducted a retrospective study of children 4 population (OR 1.7, 95% CI: 1.3–2.7; p < 0.001) with the greatest increase in p = 0.018). Failure to administer adrenaline was reduced in 2013–2017 (p = 0.007). Food was the leading anaphylaxis trigger (97.85%).Conclusion: This is the first study to suggest an increase in the incidence and severity of ED anaphylaxis presentations in children aged <2 years. Increased awareness of specific characteristics in this age group is required to facilitate timely recognition and optimal management. Further large‐scale studies are warranted to understand underlying environmental drivers and find prevention strategies to reduce the burden of disease.

The dramatic increase in the prevalence of allergic disease in recent decades reflects environmental and behavioural changes that have altered patterns of early immune development. The very early onset of allergic diseases points to the specific vulnerability of the developing immune system to environmental changes and the development of primary intervention strategies is crucial to address this unparalleled burden. Vitamin D is known to have immunomodulatory functions. While allergic disease is multifactorial, associations with reduced sunlight exposure have led to the hypothesis that suboptimal vitamin D levels during critical early periods may be one possible explanation. Interventions to improve vitamin D status, especially in early life, may be the key to allergic disease prevention.

The dramatic rise in allergic disease has occurred in tandem with recent environmental changes and increasing indoor lifestyle culture. While multifactorial, one consistent allergy risk factor has been reduced sunlight exposure. However, vitamin D supplementation studies have been disappointing in preventing allergy, raising possible independent effects of ultraviolet (UV) light exposure. The aim of this study was to examine whether UV light exposure influences the development of allergic disease in early childhood. Direct sunlight exposure (290–380 nm) in early infancy was measured via UV dosimeters. Outdoor exposure, sun protective behaviours, and allergy outcomes were assessed over the first 2.5 years of life with clinical assessment appointments at 3, 6, 12 and 30 months of age. Children with eczema had less (p = 0.038) direct UV light exposure between 0–3 months of age (median (IQR) 747 (473–1439) J/m²) than children without eczema (median (IQR) 1204 (1717–1843) J/m²); and less outdoor exposure time (7 min/day) between 11 a.m. and 3 p.m. compared to children without eczema (20 min/day, p = 0.011). These associations were seen independent of vitamin D status, and after adjusting for other potential confounders. Whilst we could not find any associations between direct UV light exposure and other allergic disease outcomes, exposure to UV light appears to be beneficial in reducing the risk of eczema development in early childhood. Further research is required to determine optimal levels of UV light exposure while balancing the potential risks.

Lower vitamin D status at birth and during infancy has been associated with increased incidence of eczema and food allergies. The aim of this study was to investigate the effect of early infancy vitamin D supplementation on allergic disease outcomes in infants at “hereditary risk” of allergic disease, but who had sufficient vitamin D levels at birth. Here, we report the early childhood follow-up to 2.5 years of age of “high-risk” infants who participated in a double-blinded, randomized controlled trial. For inclusion in this trial, late gestation (36–40 weeks) maternal 25-hydroxyvitamin D levels needed to be ≥50 nmol/L. Infants were randomized to either oral vitamin D supplementation of 400 IU/day (n = 97) or a placebo (n = 98) for the first six months of life. Vitamin D levels and allergic disease outcomes were followed up. There were no statistically significant differences in incidence of any medically diagnosed allergic disease outcomes or allergen sensitization rates between the vitamin D-supplemented and placebo groups at either 1 year or at 2.5 years of age. In conclusion, for “allergy high-risk” infants who had sufficient vitamin D status at birth, early infancy oral vitamin D supplementation does not appear to reduce the development of early childhood allergic disease.