International Archives of Allergy and Immunology最新文献

Introduction: Atopic dermatitis (AD) is a chronic inflammatory skin disorder that may progress to asthma and/or allergic rhinitis (AR) in children, a progression known as the "atopic march."

Methods: This study aimed to evaluate the natural history of AD, its clinical phenotypes, and the risk of progression to atopic march over a 10-year period. A retrospective review of medical records was performed for children diagnosed with AD and those with respiratory allergies who had prior AD. Patients were categorized into early transient, early persistent, and late-onset phenotypes based on eczema onset age and disease course. Disease progression, atopic march development, and related risk factors were analyzed.

Results: The study included 894 children (375 females, 519 males) with a mean presentation age of 3.54 ± 3.31 years, mean follow-up of 3.65 ± 2.84 years. Based on clinical phenotypes, 61% (n = 545) were early transient, 15.2% (n = 136) early persistent, and 23.8% (n = 213) late-onset. Asthma and AR rates were 8.6-11.2% in early transient, 14.0-22.8% in early persistent, and 16.0-24.9% in late-onset phenotypes, respectively. Overall, 29.9% (n = 267) exhibited the atopic march; 56.3% (n = 503) were in remission; and 43.7% (n = 391) had persistent AD. Aeroallergen sensitization was significantly associated with persistent disease (p = 0.016) and atopic march progression (p = 0.001). Family history of atopy correlated with disease persistence (p = 0.033).

Conclusion: Nearly one-third of children with AD are at risk of developing additional allergic diseases constituting the atopic march. Children with AD who exhibit aeroallergen sensitization should be closely monitored for the development of respiratory allergies.

Introduction: Relapse after omalizumab discontinuation in chronic spontaneous urticaria (CSU) is frequent, but predictors of recurrence remain unclear. This study aimed to identify clinical and laboratory factors associated with relapse within 12 months after treatment withdrawal.

Methods: We retrospectively analyzed 176 adult CSU patients who received omalizumab for ≥6 months and were followed for ≥12 months after discontinuation. Demographic, clinical, and laboratory variables were compared between relapse and non-relapse groups using logistic regression analyses.

Results: Relapse occurred in 118 patients (67.0%) within 12 months after omalizumab discontinuation. In multivariable analysis, three variables were independently associated with relapse: lower baseline Urticaria Control Test (UCT) score (odds ratio [OR] per 1-point increase = 0.60; 95% confidence interval [CI]: 0.47-0.77; p < 0.001), longer time to response after omalizumab initiation (OR per month = 2.64; 95% CI: 1.36-5.12; p = 0.004), and a history of prior relapse after treatment withdrawal (OR = 9.80; 95% CI: 1.52-63.14; p = 0.016). In univariate analysis, urticaria duration was significantly longer in relapsing patients (p < 0.001), but it was not an independent predictor. Additionally, no independent associations were found for age, sex, treatment duration, total immunoglobulin E, anti-thyroid peroxidase antibody, or comorbidities (all p > 0.05). The multivariable model showed excellent discrimination (area under the curve = 0.90; 95% CI: 0.84-0.95).

Conclusion: Lower baseline disease control, delayed clinical response, and prior relapse history were independent predictors of recurrence within 12 months after omalizumab discontinuation, whereas treatment duration and routine serologic markers were not. These findings highlight the need for individualized discontinuation strategies in CSU management.

Introduction: Fish is a potent allergen source that can induce both IgE-mediated and non-IgE-mediated reactions, particularly food protein-induced enterocolitis syndrome (FPIES). Prevalence and clinical course of fish allergy vary by age and geographic region, with limited data on tolerance development. This study aims to compare clinical and laboratory characteristics of IgE- and non-IgE-mediated fish allergy in children and to identify factors influencing tolerance.

Methods: This study included 47 children (6 months-18 years) diagnosed with fish allergy from 2010 to 2023 at a tertiary pediatric allergy clinic. Classification into IgE and non-IgE groups was based on clinical presentations, skin prick test (SPT), and specific IgE (sIgE). Tolerance was defined by negative oral food challenge (OFC) and dietary reintroduction.

Results: Among 47 patients (25 IgE-mediated, 22 non-IgE/FPIES), reactions included FPIES (46.8%), anaphylaxis (27.7%), and urticaria/angioedema (25.5%). Seven IgE and three non-IgE patients were excluded due to parental refusal of OFC. OFCs were not done in 9 IgE patients with high sIgE/SPT. OFCs confirmed tolerance in all tested IgE (9/9) and 7/17 non-IgE patients. Age at tolerance was similar between the groups. Severe reactions, inhalation-related symptoms, multiple fish allergies, and large SPT wheals predicted lower tolerance in IgE group (respectively, p = 0.028, p = 0.002, p = 0.046, p = 0.030), while older age at last reaction predicted persistence in non-IgE group (p = 0.017). Anchovy and salmon were most tolerated.

Conclusion: This first study evaluating IgE- and non-IgE-mediated fish allergies with OFCs shows substantial tolerance rates, highlighting the need for timely OFCs and personalized care addressing psychosocial factors like anxiety.

Introduction: Allergic asthma is a chronic inflammatory airway disease driven by the cytokine interleukin-13 (IL-13). Although IL-13 signals through the canonical JAK1/TYK2/STAT6 pathway, our understanding of the totality of IL-13-induced signaling intermediates is incomplete.

Methods: To address this, we performed a phospho-proteomic analysis of IL-13-stimulated A549 human airway epithelial cells. IL-13 stimulation led to differential phosphorylation at 145 unique serine/threonine residues across 92 proteins involved in diverse cellular processes. In silico analysis was used to predict kinases responsible for the observed changes, and therapeutics which may reduce IL-13-mediated pathology. The activation of these kinases and the ability of these therapeutics to limit IL-13 activity were tested in vitro using molecular techniques and in vivo in an IL-13-induced model of asthma.

Results: Analysis of IL-13-induced differentially phosphorylated proteins revealed activation of several pathways including RNA splicing, cytoskeletal remodeling, GTPase activity, and focal adhesion complex formation. Network analysis identified SRC family kinases (SFKs), a family of non-receptor tyrosine kinases, as potential regulators of IL-13-induced changes in phosphorylation, and dasatinib, a pan-SFK inhibitor, as a potential inhibitor of IL-13 signaling. In both human and mouse lung fibroblasts, molecular approaches demonstrated activation of SFKs following IL-13 stimulation. In vitro, dasatinib reduced IL-13-induced STAT6 phosphorylation and downstream gene expression. In vivo, dasatinib attenuated IL-13-induced airway hyperresponsiveness without significantly affecting inflammatory cell infiltration or gene expression in bronchoalveolar lavage fluid.

Conclusion: These findings support a potential therapeutic role for dasatinib in inhibition of IL-13-driven responses such as those observed in allergic asthma.

Introduction: Several biological treatments are available for patients with asthma who are not well controlled with inhaled corticosteroids (ICS) and bronchodilators. Real-life studies comparing the effectiveness of add-on biological treatments are lacking.

Methods: In this retrospective study, the population included adult patients with asthma who were treated with omalizumab and mepolizumab. The number of systemic corticosteroids (injectable and oral) and the number of ICS purchases were compared between 12 months before the first biological treatment and 12 months after.

Results: Of 173 patients, 122 were treated with omalizumab and 51 with mepolizumab. A higher proportion of females received mepolizumab than omalizumab (87% vs. 48%, respectively, p = 0.034). Omalizumab significantly reduced the number of patients who purchased corticosteroid injections from 34% to 21% (p < 0.001) but not mepolizumab. A trend toward reduction in the number of patients who purchased corticosteroid tablets was demonstrated during the year of mepolizumab treatment (from 84% to 63%, p = 0.07). For both drugs, no significant differences were found in the mean number of corticosteroid injections, tablets, and inhaler purchases between the year before and during the biological treatments.

Conclusion: Omalizumab was superior to mepolizumab in reducing the number of patients who were treated with corticosteroid injections.

Introduction: The aim of this study was to conduct a network meta-analysis (NMA) of randomized controlled trials (RCTs) to compare the efficacy of various biologics for treating moderate-to-severe allergic asthma.

Methods: This study conducted a comprehensive and systematic literature search in Cochrane Library, Embase, PubMed, and Web of Science databases from the inception to December 31, 2024. The data extracted from eligible literature were analyzed using the Cochrane Randomized Trials Risk of Bias 2 tool and Stata 18.0 program.

Results: A total of 19 RCTs, involving 7,449 patients with moderate-to-severe allergic asthma, were included in this NMA. In terms of reducing exacerbations, benralizumab (mean difference (MD) = -0.47, 95% confidence interval (CI) [-0.82, -0.12]), dupilumab (MD = -0.47, 95% CI [-0.72, -0.21]), omalizumab (MD = -0.30, 95% CI [-0.42, -0.17]), and tezepelumab (MD = -0.81, 95% CI [-1.09, -0.54]) all demonstrated superior efficacy compared to placebo. Additionally, tezepelumab was markedly more advanced than omalizumab (MD = -0.52, 95% CI [-0.80, -0.23]). With regard to lung function improvement, dupilumab (MD = 0.16, 95% CI [0.07, 0.24]) and tezepelumab (MD = 0.08, 95% CI [0.03, 0.14]) both exceeded placebo. Regarding asthma control, dupilumab (MD = -0.40, 95% CI [-0.77, -0.04]) and omalizumab (MD = -0.49, 95% CI [-0.89, -0.08]) both effectively lowered scores on the asthma control questionnaire (ACQ) compared to placebo. For enhancing quality of life, omalizumab (MD = 0.62, 95% CI [0.21, 1.03]) significantly raised scores on the standardized asthma quality of life questionnaire (AQLQ [S]+12) relative to placebo.

Conclusion: Considering its significant clinical advantages in reducing exacerbations and improving lung function, tezepelumab should be prioritized as a treatment option for moderate-to-severe allergic asthma.

Introduction: The aim of the study was to analyze the risk factors for vitiligo complicated with autoimmune thyroid disease (AITD) and establish a nomogram prediction model.

Methods: Clinical data of 304 vitiligo patients admitted to our hospital from February 2023 to January 2025 were collected. Logistic regression was used to identify independent risk factors for vitiligo complicated with AITD. A nomogram prediction model was constructed using the rms package in R (R3.5.3). Internal validation was performed via 1,000 repeated samplings using the Bootstrap method in the caret package. The consistency index (C-index) was calculated using the rms package, and the receiver operating characteristic curve was plotted using the ROCR and rms packages.

Results: The incidence of AITD in vitiligo patients was 17.76%. Hyperglycemia, a long disease duration of vitiligo (≥5 years), non-segmental vitiligo type, negative emotion, smoking, family history of AITD, and family history of other autoimmune diseases were identified as independent risk factors (all p < 0.05). The nomogram model based on these risk factors showed good consistency between observed and predicted incidences (Hosmer-Lemeshow test: χ2 = 3.920, p = 0.709), with a high C-index of 0.858 (95% confidence interval: 0.830-0.886).

Conclusion: Vitiligo patients, especially those with risk factors, should be screened for AITD whenever possible. The developed nomogram provides a practical tool for clinicians to identify high-risk individuals, facilitating tailored screening and early intervention strategies.

Introduction: The global burden of respiratory allergic diseases linked to outdoor allergens remains poorly quantified despite increasing evidence of the allergens' impacts on respiratory allergic diseases. This systematic review synthesizes epidemiological evidence on the association between exposure to outdoor airborne allergens and respiratory disease incidence.

Methods: Following PRISMA 2020 guidelines, we systematically searched three databases, PubMed, Embase, and the Cochrane Library, until December 2024. Observational studies reporting effect estimates for respiratory outcomes (asthma, allergic rhinitis, COPD exacerbations, and cough) associated with quantified outdoor allergen exposure were eligible. Two reviewers independently conducted screening, data extraction, and quality assessment using an adapted Newcastle-Ottawa Scale (NOS). Random-effects models were employed to pool odds ratios (ORs), with subgroup analyses by sex. Publication bias was evaluated using Begg's and Egger's tests, respectively.

Results: From 6,551 identified records, 7 articles with 70 studies (46,325 participants across 3 countries) met the inclusion criteria. High-quality studies (NOS ≥7) constituted 86% of the included articles. Pooled analyses revealed significant associations between outdoor allergen exposure and respiratory outcomes: OR = 1.03 (95% confidence interval [CI]: 1.01-1.04; p = 0.008). Egger's publication bias was non-significant (Egger's p = 0.21), and Begg's publication bias was also non-significant (Begg's p = 0.31). Trim-and-fill funnel plots suggested possible missing small-null studies, but the statistical analysis was non-significant. Sensitivity analyses confirmed robustness when excluding studies with potential residual confounding (pooled OR range: 1.02-1.06). Subgroup analyses demonstrated that the female subgroup, rather than the male subgroup, got stronger effects significantly: OR = 1.04 (95% CI: 1.01-1.07), compared with the male subgroup OR = 1.02 (95% CI: 0.99-1.04).

Conclusions: This comprehensive synthesis provides high-quality evidence that outdoor allergen exposure significantly increases risks of respiratory allergic disease. The female is more likely to get respiratory morbidity compared with the male. Further research should prioritize harmonized exposure metrics and evaluate interactive effects with anthropogenic air pollutants.

Introduction: In the sub-Saharan area, data regarding total IgE levels particularly among apparently healthy population remain rare. Defining the IgE profile is crucial to identify allergic diseases driven by westernized lifestyles as elevated IgE may compromise safety of blood transfusion. The aim of the study was to assess total IgE levels in blood donors, investigate a possible correlation with sociodemographic, environmental, and biological parameters such as parasitic infestation and discuss their implications for public health and allergy in West Africa.

Methods: We carried out a prospective cross-sectional, descriptive and analytical study among blood donors. Information on the participants' allergy history as well as relevant environmental exposures were collected. Total IgE determination was performed by chemiluminescence, and stool samples underwent parasitological examination.

Results: More than 30% of the donors had elevated total IgE. Stool parasite examinations were positive in 18% of blood donors with 2% helminthiasis. There was a significant relationship between age (p = 0.00, correlation coefficient = -0.22), eosinophil count (p = 0.003, correlation coefficient = -0.60), and total IgE indicating that age and eosinophils counts are associated with increased total IgE concentrations. Highest median of total IgE levels was seen in parasitized people regardless of atopic status supported the idea that parasitic infection is an important factor of total IgE level.

Conclusion: Continuing assessments are important to understand these high levels of IgE in blood donors. Since elevated total IgE can also occur in non-allergic state, we need to integrate surveillance strategies that address both parasitic infections and allergic diseases completed by others relevant investigations for more comprehensive approach in West Africa.

Background: Allergic diseases represent a growing public health challenge due to aberrant immune responses to harmless environmental substances. Natural compounds have emerged as potential modulators of these responses. Cinnamon, a widely used spice with a rich profile of bioactive constituents, has demonstrated notable anti-inflammatory and immunomodulatory properties. This narrative review aimed to synthesize current in vitro and in vivo evidence regarding the effects of cinnamon and its derivatives on allergic disease mechanisms.

Summary: This narrative review compiles and critically examines findings from experimental studies that investigated the influence of cinnamon on key immunologic processes involved in allergic conditions. The review focuses on the modulation of antigen presentation by dendritic cells and macrophages, alterations in T-cell responses, mast cell stabilization, and the attenuation of airway and skin inflammation. Evidence from various experimental models was integrated to elucidate the molecular pathways affected by cinnamon. The reviewed studies indicate that cinnamon extract can reduce antigen-presenting cell maturation by decreasing co-stimulatory molecule expression and suppressing pro-inflammatory cytokine production. Additionally, cinnamon appears to stabilize mast cells by impairing receptor binding and disrupting calcium signaling, leading to a reduction in histamine release and other inflammatory mediators. Evidence further suggests that cinnamon modulates T-cell responses by promoting a regulatory immune cell profile and diminishing overall cytokine secretion. In experimental models of respiratory and skin allergies, treatment with cinnamon or its active compounds was associated with decreased inflammatory cell infiltration, improved airway function, and reduced severity of dermatitis-like lesions.

Key messages: The collective evidence from experimental studies suggests that cinnamon holds promise as a natural, multi-target therapeutic agent in managing allergic diseases. Its ability to modulate antigen presentation, stabilize mast cells, and promote regulatory immune responses supports its potential use as an adjunctive treatment for conditions such as asthma, allergic rhinitis, and atopic dermatitis. Further clinical investigations are warranted to optimize dosing strategies, formulations, and long-term safety for its practical application in allergic disease management.