Clinical and Translational Allergy最新文献

To the Editor,

Allergen immunotherapy (AIT) remains a well-established and widely used approach for treating immediate type allergies including allergic rhinitis and conjunctivitis, certain forms of allergic asthma, select food allergies, and allergic reactions to Hymenoptera insect venom immunotherapy (VIT). Currently, VIT is the only causative and, in some cases, can be life-saving.¹

AIT has been proven to be effective for most age groups, including patients over 60 years old.² However, limited studies have confirmed the safety and effectiveness of VIT in these populations.² This is particularly important in cases of anaphylactic reactions following an insect sting, which is an indication for VIT also in the oldest patients.³

Therefore, evaluating of the effectiveness of VIT and the rate at which tolerance to the venom develops is of key importance. The basophil activation test (BAT) can be the optimal tool for such an evaluation. The BAT is a valuable tool for final qualification for VIT and often resolves doubts.^{4, 5} The most diagnostically valuable method for assessing the effectiveness of VIT is the live insect sting challenge (SP). However, SP has significant limitations, including the necessity of conducting it in highly specialized centers, the risk of complications, including those related to the application of the full, unfractionated dose of the allergen, and the potential risk of reactivating the allergic state. Unlike SP, the BAT for assessing VIT effectiveness is free of these limitations.⁶

The authors would like to present an assessment of the efficacy of VIT for wasp venom after 1 year of treatment in different age groups, comparing the efficacy in young and old patients to identify potential differences. This builds of an earlier observational study, which confirmed comparable efficacy after 6 months of VIT initiation in people aged 18–35 and over 60 years in the BAT test.⁷ These results were independent of the type of vaccine used Venomenhal (Hal Allergy) or Diater.

In the second part of observation, the study group was slightly reduced (drop-out due to patients' resignation despite the effectiveness of the treatment and the lack of adverse effects), and its final characteristics are presented in Table 1.

The methodology of the BAT assessment and the entire study protocol were described and consistent with the published first part of the study.⁷

The effectiveness of VIT was evaluated using BAT, revealing a statistically significant decrease in CD63 reactivity in the mean of about 86%–88% from the base for older patients similarly, as in young 84%–85% (p > 0.05) after 6 months of VIT. Similar trends were observed after next 6 months, and a comparable decrease in basophil activity was ma

Background: Anaphylaxis is an acute, severe, and potentially fatal reaction marked by the fast onset of symptoms and organ involvement that may lead to death from vascular collapse or airway obstruction. Despite adrenaline (epinephrine) being the first-line medication for reversing anaphylactic symptoms, misconceptions about its safe and correct use persist and lead to improper administration.

Methods: This review provides a comprehensive overview of clinical use of adrenaline autoinjectors (AAIs) in the management of anaphylaxis, key safety considerations, and pharmacokinetic/pharmacodynamic profile of three of the currently marketed AAIs.

Results: When administered intramuscularly (IM) at the recommended dose for anaphylaxis, adrenaline is considered safe; however, adequate training in emergency care is essential to minimize dosage errors and mitigate safety risks. In specific situations, such as refractory anaphylaxis, intravenous (IV) administration is advised under specialized settings due to the potential risk of severe cardiovascular complications that can result from dosing errors.

Conclusion: Although adrenaline can cause mild and transient side effects even when administered correctly at the recommended dosage, the potential side effects should not deter its use in critical situations such as anaphylaxis. This review aims to highlight the role of AAIs in improving patient outcomes during anaphylactic emergencies.

Background: Robust data are essential for clinical and epidemiological research, yet in chronic spontaneous urticaria (CSU), certain patient groups, such as the elderly or comorbid patients, are often underrepresented. In clinical trials, strict inclusion and exclusion criteria frequently limit recruitment, making it difficult to achieve sufficient statistical power. Similarly, real-world observational studies may lack sufficient sample sizes for robust analysis. To address these limitations, we generated synthetic patient data that reflect these groups' clinical characteristics and variability. This approach enables more comprehensive analyses, facilitates hypothesis testing in otherwise inaccessible populations, and supports the generation of evidence where traditional data sources are insufficient.

Methods: A tree-based decision model was applied to generate synthetic data based on an existing set of real-world data (RWD) from the Chronic Urticaria Registry (CURE). Descriptive characteristics and association strength between relevant RWD variables and their synthetic counterparts were analyzed as indicators of replication accuracy, providing insight into how closely the synthetic data aligns with the RWD. Finally, we determined the minimum sample size required to generate high-quality synthetic data.

Results: The algorithm produced extensive synthetic data records, closely mirroring patient demographics and disease clinical characteristics. Smaller subgroups of the data were equally replicated and followed the same distribution as RWD. Known associations and correlations between disease-specific factors (disease control) and risk factors (age) yielded similar results, with no significant difference (p > 0.05). The lowest threshold at which synthetic data could be generated while maintaining high accuracy in RWD was identified to be 25%, enabling a fourfold increase in the synthetic population.

Conclusion: Synthetic data could replicate RWD with reasonable accuracy for patients with CSU down to 25% of the original population size. This method has the potential to extend small patient subgroups in clinical and epidemiological research.

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by tissue eosinophilia and itch. We evaluated the effect of eosinophil depletion with benralizumab on markers of inflammation in the skin of patients with AD.

Methods: After a 4-week washout from oral anti-inflammatory medications 20 patients with moderate to severe AD completed a randomized, double-blind, placebo-controlled parallel-group study comparing 3 doses q4wk 30 mg subcutaneous benralizumab to placebo. Lesional and unaffected skin biopsies were collected before and after 28 and 65 days of treatment, respectively, for quantification of eosinophils and IL-5Rα-bearing cells in papillary dermis. Histological measurements of epidermal thickness, spongiosis, neutrophilic and lymphocytic infiltration, as well as clinical scores EASI, SCORAD, IGA, DLQI, and POEM were conducted throughout the study. Outcomes were compared between placebo and benralizumab treatment groups using a Mann-Whitney U-test.

Results: Benralizumab, compared to placebo, reduced IL-5Rα+ cells and MBP+ EG2+ eosinophils in lesions and unaffected skin (p < 0.05). In skin lesions, benralizumab reduced MBP+ eosinophils and basophils but had no effect on eosinophil progenitor (EoP; CD34+ IL-5Rα+) or mast cell numbers. There was no change in other skin histological measurements or IGA scoring of the observational lesion, nor improvement in clinical scores.

Conclusion: Benralizumab treatment significantly inhibited accumulation of MBP+ eosinophils and basophils in lesional skin of patients with moderate to severe AD. However, a lack of improvement in histological and clinical outcomes suggests that other inflammatory pathways are central to the pathobiology of severe atopic dermatitis.

Trial registration: (ClincialTrials.gov number, NCT03563066).