Clinical and Experimental Allergy最新文献

Objective: Asthma and atopic dermatitis are associated with various physical and psychosocial outcomes, however, the prevalence of sexual dysfunction in these populations remains underexplored. This meta-analysis aimed to assess the prevalence of sexual dysfunction among individuals with asthma and atopic dermatitis.

Design: A systematic review and random-effects meta-analysis was conducted to estimate pooled prevalence with 95% confidence intervals (CIs). Subgroup analyses were conducted stratifying by sex, geographic regions and diagnostic tools.

Data sources: PubMed/MEDLINE, Embase, Scopus and Cochrane Library were searched from inception to 1 July 2025.

Eligibility criteria: Studies including adults with asthma or atopic dermatitis were eligible. Sexual dysfunction was defined as impairments in sexual desire or sexual response, identified via clinical diagnosis or validated questionnaires, including the Female Sexual Function Index and International Index of Erectile Function.

Results: A total of 19 studies comprising 10,851 participants, including 1577 patients with asthma or atopic dermatitis from 18 countries across five continents, were included. The pooled prevalence of sexual dysfunction was 54.3% (95% CI 45.9-64.3) in asthma and 19.1% (13.4-27.3) in atopic dermatitis. In both conditions, prevalence was substantially higher in females than males: 71.5% (95% CI 63.3-80.7) versus 29.6% (17.1-51.2) in asthma and 53.0% (36.4-77.1) versus 16.7% (7.3-38.2) in atopic dermatitis. Studies using validated tools reported higher prevalence than those relying on supportive methods or clinical diagnoses. Smoking status was not significantly associated with differences in prevalence among individuals with asthma. Among control groups, pooled prevalence was 9.7% (95% CI 0.6-169.6) for males and 30.1% (18.7-48.5) for females in asthma studies and 2.2% (0.16-28.8) overall in atopic dermatitis studies.

Conclusions: Sexual dysfunction was highly prevalent among individuals with asthma and atopic dermatitis, particularly in females. These findings highlight the need for greater clinical attention to sexual dysfunction in the management of allergic diseases.

Systematic review registration: PROSPERO (CRD420251115928).

Background: Allergy is the most common and earliest onset non-communicable disease in children. The early identification of children who are at risk of allergy would allow early intervention to prevent the onset of the disease or reduce its impact. The origins of allergy are hypothesized to be derived from early developmental events which include prenatal events and early childhood exposures. We have previously identified that many placental glucocorticoid-regulated genes were also associated with child allergy.

Objective: We have questioned if it is possible to predict which children are at risk of allergy based on their placental glucocorticoid-regulated mRNA profile.

Methods: Placentae from two different populations located in South Australia (n = 105) and Victoria, Australia (n = 261) were included in the study. Glucocorticoid regulated genes were measured by qPCR. Statistical modelling was executed in R (version 4.4.1).

Results: Evaluation of the importance of each gene in the model identified AFF1, ARID5B, IER3, ATF4 and SLC19A2 as the top five ranking genes. The best-performing random forest model achieved an AUC of 0.664, indicating moderate ability to distinguish between positive and negative allergic susceptibility. While our models demonstrate both measurable specificity and sensitivity, the glucocorticoid genes particularly excel at identifying children who will not develop an allergy.

Conclusion: This study demonstrates that placental glucocorticoid-regulated genes possess significant predictive power, especially in identifying individuals unlikely to develop allergies. It offers further evidence that the placentae of nonallergic children and allergic children are transcriptionally distinct.

Objective and design: This systematic review compared the scope, purpose, and recommendations of internationally published penicillin allergy delabelling guidelines (PADLGs) and assessed their quality using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) instrument.

Data sources: A systematic search of MEDLINE, EMBASE, and CINAHL databases, and Google, Google Scholar, websites of professional allergy societies (n = 95), and guideline repositories (n = 16) was conducted to August 2024.

Eligibility criteria: Any document that reported itself as being an evidence-based guideline, practice guideline, expert recommendation, consensus statement, position paper, or practice parameter for penicillin allergy delabelling ('PADL-G') was eligible for inclusion. Only those developed for use by health care professionals were included. Guidelines for community or patient use and hospital protocols or fact sheets were excluded.

Results: Eighteen guidelines published between 2014 and 2024 were identified, representing 12 countries across four regions. PADLGs varied in scope, target users, and clinical recommendations, both within and across clinical settings. Most provided recommendations for risk stratification, testing, and delabelling methods, with many supporting direct delabelling/direct challenge in low-risk patients. Substantial variation was observed in risk assessment tools, eligibility criteria, and post-test delabelling strategies. Overall, the quality of PADLGs was low, with only two meeting predefined high-quality criteria. Critical gaps included limited methodological rigour, poor stakeholder involvement, and lack of guidance for real-world implementation.

Conclusions: To support safe and scalable PADL approaches, clearer, more consistent, and methodologically robust guidelines are needed to address the global burden of inappropriate penicillin allergy labels.

Systematic review registration: The protocol for this review was prospectively registered at Open Science Framework: osf.io/9fvr7.

Background: People with hereditary angioedema (HAE) experience anxiety from the unpredictable nature of attacks and the burden of parenteral on-demand therapies, potentially leading to delays or avoidance of treatment. This analysis assessed factors associated with anxiety during attacks and the impact of oral sebetralstat versus placebo on anxiety in the KONFIDENT trial.

Methods: Participants in the randomised, double-blind, phase 3 KONFIDENT trial (NCT05259917) treated attacks with sebetralstat 300 mg, 600 mg or placebo as early as possible after onset. Anxiety was recorded at treatment administration, every 0.5 h thereafter through 4 h, hourly from 5 to 12 h and every 2 h from 14 to 24 h using an 11-point modified General Anxiety Numeric Rating Scale (GA-NRS). Prespecified exploratory endpoints assessed in all attacks and in attacks rated as inducing moderate-to-extreme anxiety (GA-NRS ≥ 4) included cumulative GA-NRS score and meaningful reduction in anxiety (defined as ≥ 2-point reduction in GA-NRS for ≥ 2 consecutive timepoints); least squares mean change from treatment administration in GA-NRS at 4 and 12 h was also assessed. This study was sponsored by KalVista Pharmaceuticals.

Results: Overall, 115 (44%) attacks were rated as inducing moderate-to-extreme anxiety. Female sex, shorter time since HAE diagnosis and greater attack severity were associated with greater anxiety at treatment administration. Reduction in cumulative anxiety after sebetralstat use was significantly greater versus placebo. The time to meaningful reduction in anxiety endpoint showed agreement with time to beginning of symptom relief, reduction in attack severity and complete attack resolution endpoints.

Conclusion: Moderate-to-extreme anxiety was common in HAE attacks. Reduction in anxiety was significantly greater in attacks treated with sebetralstat compared with placebo.