Journal of Investigational Allergology and Clinical Immunology最新文献

Asthma, a prevalent chronic respiratory disease, manifests in heterogeneous phenotypes and endotypes, necessitating bespoke therapeutic approaches. Asthma exacerbations are characterized by worsening of symptoms and decline in lung function and present substantial challenges despite advances in understanding and treatment. Viral respiratory infections, notably those caused by rhinovirus, serve as primary triggers, with allergic sensitization and environmental exposures increasing susceptibility. Deficient antiviral responses in asthmatic airway epithelial cells, particularly impaired interferon production, perpetuate inflammation and hyperresponsiveness, contributing to exacerbations. Additionally, genetic polymorphisms influence host responses and susceptibility. Recent studies underscore the association between specific inflammatory profiles, particularly eosinophil-mediated inflammation, and the frequency of exacerbations. Biologic therapies targeting inflammatory pathways show promise in reducing the frequency of exacerbations, thus underscoring the importance of understanding inflammatory phenotypes when selecting treatment. Notably, T2 inhibitors may modulate immune responses, potentially mitigating viral exacerbations. Characterizing exacerbations is crucial for optimizing therapeutic strategies. Evidence suggests a dissociation between baseline inflammatory profiles and exacerbation phenotypes, highlighting the need for individualized management. Phenotyping exacerbations using sputum analysis helps to identify predominant inflammatory patterns and thus inform treatment decisions. The varied responses to biologic therapies further emphasize the importance of phenotyping exacerbations in refining treatment algorithms. In conclusion, phenotyping asthma exacerbations provides valuable insights into underlying inflammatory mechanisms and enables personalized therapy. Understanding the complex interplay between viral triggers, inflammatory pathways, and responses to treatment is essential if we are to effectively manage severe asthma and reduce the burden of exacerbations. Further research into the mechanistic actions of biologic therapies in mitigating viral exacerbations is warranted to optimize asthma management strategies.

Background: The safety profile of venom immunotherapy (VIT) is a relevant issue, and considerable differences have been reported in the safety and efficacy of this treatment modality. The primary aim of this study was to evaluate the safety of angiotensin-converting enzyme inhibitors and ß-blockers during VIT. In a second analysis, we evaluated data on premedication and venom preparations and their association with systemic adverse events (AEs) during the up-dosing phase and the first year of the maintenance phase, as well as the outcome of field stings and sting challenges.

Methods: Ours was an open, prospective, observational, multicenter study that recruited 1425 patients, of whom 1342 underwent VIT.

Results: Premedication with oral antihistamines was taken by 52.1% of patients during up-dosing and 19.7% of patients during the maintenance phase. Antihistamines had no effect on the frequency of systemic AEs (P=.11), although large local reactions (LLRs) were less frequent (OR, 0.74; 95%CI, 0.58-0.96; P=.02). Aqueous preparations were preferred for up-dosing (73.0%), and depot preparations were used for the maintenance phase (64.5%). The type of venom preparation had no influence on the frequency of systemic AEs or on the effectiveness of VIT (P=.26 and P=.80, respectively), while LLRs were less frequent with depot preparations (P<.001).

Conclusions: Pretreatment with oral antihistamines during VIT significantly reduces the frequency of LLRs but not systemic AEs. All venom preparations were equally effective and did not differ in terms of the frequency of systemic AEs.

Background: The usefulness of the mast cell activation test (MAT) in diagnosing patients with uninterpretable basophil activation test (BAT) results caused by nonresponding basophils has not been addressed. Our study evaluated whether the results of the MAT were associated with the severity of the allergic reaction.

Methods: We recruited 39 patients with Hymenoptera venom allergy (HVA), 22 nonsensitized controls, and 37 BAT nonresponding HVA patients. Specific IgE levels for honeybee venom (HBV) and yellow jacket venom (YJV) and total IgE were quantified using the IMMULITE® system. We performed a BAT and a MAT, which was based on the response of LAD2 cells to HBV and YJV.

Results: We first optimized the susceptibility of LAD2 cells to IgE-mediated degranulation in HVA and showed that prestimulation with IL-33 and IL-6 significantly increased the responsiveness of LAD2 cells to allergen stimulation (P<.01). The LAD2 MAT results correlated with the BAT results, and patients with severe sting reactions (Mueller grades III and IV) had a median 2-fold higher LAD2 MAT score than patients with nonsevere sting reactions (large local reaction or Mueller grades I and II) (P<.05). Furthermore, LAD2 MAT provided conclusive results in 20 of the 37 HVA patients (54.1%) with nonresponding basophils in the BAT.

Conclusions: The LAD2 MAT is a new diagnostic tool for HVA patients with nonresponding basophils. LAD2 MAT can identify patients at risk of severe sting reactions and can thus help guide recommendations for venom immunotherapy and improve the management of patients with HVA.

Background and objectives: Sunflower seed is one of the most common edible seeds. Its consumption is growing. Cases of sunflower seed allergy have been reported since the 1970s. However, there are few data on the prevalence and clinical manifestations of sunflower seed allergy. To improve our understanding of sunflower seed allergy.

Methods: We evaluated the clinical and immunological features of patients with sunflower seed allergy diagnosed in the allergy department of a tertiary hospital in Madrid over a 5-year period.

Results: Forty-seven patients reported adverse reactions after ingestion of sunflower seed and were sensitized specifically to sunflower seed, as determined by skin prick test (median, 8 mm) or specific IgE (median, 1.10 kUA/L). Most reactions were adult-onset and were preceded by a history of atopy and other food allergies, predominantly to peach, peanut, and nuts. The clinical presentation of sunflower seed allergy ranged from mild to severe, with many patients experiencing severe reactions, in which epinephrine was underused. Repeated exposures to sunflower seed in the same patient showed severity of symptoms to vary. Levels of sunflower seed IgE were strongly correlated with levels of IgE to nonspecific lipid transfer proteins, while the severity of the reactions did not differ significantly according to sensitization to the proteins.

Conclusion: Our findings reveal variability in the clinical presentations of sunflower seed allergy on repeated exposures and underuse of epinephrine in anaphylaxis. We highlight the importance of strict avoidance of sunflower seed and accurate prescription and administration of epinephrine in allergic patients.

Interest in finding efficient ways to remove penicillin allergy alerts has grown as a result of awareness of the considerable excess of falsenegative diagnoses in patients with penicillin allergy labels (90%-95%), the poorer course with non-ß-lactam antibiotics, the increase in bacterial resistance, and the fact that these problems can affect up to 20% of the population in some countries. The strategies proposed have generated many publications in countries where the number of allergists to conduct such studies is low. In many cases where delabeling is performed, the risk of ß-lactam allergy is low, and a single penicillin challenge is sufficient to delabel the alert. However, other less "ultrarapid" strategies can be used to administer a ß-lactam during an admission for infection and thus postpone delabeling until traditional drug allergy consultations. However, the definitive withdrawal of ß-lactam alerts is threatened by nonremoval of alerts in electronic health records and by the reactivation or nonsynchronization of alerts between electronic systems at different levels of care. Allergy departments need to reflect on how to implement practices that enable rapid and efficient delabeling of drug allergy alerts, especially in patients with major comorbidities.