Clinical and Experimental Allergy最新文献

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.

Background: During the grass flowering season, fungal spores are abundant in outdoor air. We tested for co-sensitisations to grass pollen and fungal spores, assessed the degree of co-exposure, and studied its impact on the nasal mycobiome and immune responses.

Methods: Fungi-specific IgE-levels were studied in 277 individuals with and without grass pollen sensitisation. In a small cohort (n = 7), exposure to grass pollen and fungal spores was monitored during 5 consecutive indoor and outdoor stays in a flowering meadow and correlated with changes in the nasal mycobiome. Cytokines of nasal epithelial cells were studied under stimulation with recombinant grass pollen allergens, with and without fungal spores derived from outdoor isolates.

Results: IgE-sensitisation against the studied fungi was significantly more frequent among individuals with grass pollen sensitisation than among those without grass pollen sensitisation. Outdoor exposure resulted in changes in the nasal mycobiome, with a transitory enrichment of environmental fungi, for example, Cladosporium species. Most of the fungi cultivated from outdoor air samples belonged to the genera Fusarium, Cladosporium and Penicillium. Apical co-stimulation of nasal epithelial cells with grass pollen allergens and Fusarium, Cladosporium or Penicillium spores led to an increased loss of transepithelial electrical resistance and induction of pro-inflammatory cytokine release compared to mono-stimulation.

Conclusion: Frequent co-exposure to fungal spores and grass pollen may increase the chance of acquiring a co-sensitisation to both allergens. Environmental fungi interact with and transitorily change the local mycobiome. Under co-exposure, fungal spores induce nasal inflammation and foster immune responses to otherwise poorly immunogenic pollen allergens.

Background: Chronic urticaria (CU) diagnosis includes the patient's clinical history and physical examination. However, atypical presentations or misdiagnosis can lead to diagnostic delay (DD).

Objective: The impact and contributing factors of DD in CU are unknown and were assessed in the present study.

Methods: We retrospectively analysed data from CU adult patients from the international, multicenter Chronic Urticaria Registry (CURE).

Results: Of 4332 CU patients, 61% had standalone chronic spontaneous urticaria (sCSU), 18% had ≥ 1 form of chronic inducible urticaria (CIndU), and 21% had a combination of both (CSU + CIndU). Diagnosis of CU was delayed in 24% of patients by at least 1 year. CIndU patients showed a longer DD compared to those with sCSU or CSU + CIndU (median, [IQR]: 4, [0-22] vs. 1, [0-6] vs. 2, [0-9] months, p < 0.001). Among CIndU patients, symptomatic dermographism (n = 264) and cholinergic urticaria (n = 103) patients had the longest DD compared to all other CIndU subgroups (median: 4 months, p = 0.005 for both). In CIndU patients, a longer DD was associated with having an additional CIndU (OR: 12.8, p = 0.03), younger age, comorbidities, lower disease control, and lack of second-generation H₁-antihistamine treatment. In CSU patients, a DD of ≥ 6 months was associated with lower CSU activity (median weekly Urticaria Activity Score of 14 vs. 21, p = 0.02) compared to that of DD < 6 months.

Conclusions: Diagnosis of CU is delayed in one out of four patients. Greater awareness of the guideline-recommended CU classification, clinical presentation, and diagnostic work-up can facilitate CU diagnosis.