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Background Routine immunization, one of the most effective public health interventions, has effectively reduced death and morbidity due to a variety of infectious diseases. However, allergic reactions to vaccines occur very rarely and can be life threatening. Given the large numbers of vaccines administered worldwide, there is a need for an international consensus regarding the evaluation and management of allergic reactions to vaccines. Methods Following a review of the literature, and with the active participation of representatives from the World Allergy Organization (WAO), the European Academy of Allergy and Clinical Immunology (EAACI), the American Academy of Allergy, Asthma, and Immunology (AAAAI), and the American College of Allergy, Asthma, and Immunology (ACAAI), the final committee was formed with the purpose of having members who represented a wide-range of countries, had previously worked on vaccine safety, and included both allergist/immunologists as well as vaccinologists. Results Consensus was reached on a variety of topics, including: definition of immediate allergic reactions, including anaphylaxis, approaches to distinguish association from causality, approaches to patients with a history of an allergic reaction to a previous vaccine, and approaches to patients with a history of an allergic reaction to components of vaccines. Conclusions This document provides comprehensive and internationally accepted guidelines and access to on-line documents to help practitioners around the world identify allergic reactions following immunization. It also provides a framework for the evaluation and further management of patients who present either following an allergic reaction to a vaccine or with a history of allergy to a component of vaccines.

Asthma is clearly related to airway or blood eosinophilia, and asthmatics with significant eosinophilia are at higher risk for more severe disease. Eosinophils actively contribute to innate and adaptive immune responses and inflammatory cascades through the production and release of diverse chemokines, cytokines, lipid mediators and other growth factors. Eosinophils may persist in the blood and airways despite guidelines-based treatment. This review details eosinophil effector mechanisms, surface markers, and clinical outcomes associated with eosinophilia and asthma severity. There is interest in the potential of eosinophils or their products to predict treatment response with biotherapeutics and their usefulness as biomarkers. This is important as monoclonal antibodies are targeting cytokines and eosinophils in different lung environments for treating severe asthma. Identifying disease state-specific eosinophil biomarkers would help to refine these strategies and choose likely responders to biotherapeutics.

INTRODUCTION Respiratory syncytial virus (RSV) is the leading cause of severe acute lower respiratory tract infection (LRTI) in infants and young children, resulting in an estimated 33 million infections annually, >3 million hospitalizations, and >100 000 deaths in children under 5 years globally, with a mortality rate of up to 9% in low-resource countries, which have 99% of the global RSV mortality.1 RSV infection is associated with an increased risk of respiratory failure, admission to the ICU, mechanical ventilation, use of oxygen therapy, and death.2,3 Severe RSV-LRTI in early childhood increases the risk of long-term respiratory disorders such as repeated wheezing or asthma.4–6 Most children have had serologically proven RSV infection by age 2 years, representing a major healthcare burden.7,8 RSV epidemics increase health resource utilization (HRU). [...]the early arrivals of the RSV epidemic seasons during 2022 and 2023 overlapped with the coronavirus disease 2019 (COVID-19) and influenza epidemics and resulted in severe pressure and impact on the healthcare systems of multiple countries.9–12 Risk factors such as socio-economic status influence morbidity and mortality from acute RSV infection, with low- and middle-income countries being disproportionately impacted.13 Young age at time of infection is a key risk factor. A systematic analysis of the global burden of RSV mortality found that 45% of the 101 400 RSV-caused deaths in children under 5 years of age occurred in infants during the first 6 months of life and that 3.6% of all deaths among infants 2–6 months of age were caused by RSV.1 Premature infants and infants with underlying disease are at high risk for severe RSV infection; however, most of the RSV burden occurs in previously healthy infants.14,15 There is therefore a need to protect all infants from RSV infection, which can greatly reduce HRU, thereby reducing pressure on the healthcare system, especially during the RSV epidemic season. Countries will conduct evaluations in their immunization programs to ensure the accessibility of prophylactic mAbs for all infants and some young children.23–36 In view of the global burden of RSV disease among infants, in September 2024, the World Health Organization and its Strategic Advisory Group of Experts on Immunization (SAGE) recommended that “all countries introduce passive immunization for the prevention of severe RSV disease in young infants.”

In 2004 the World Allergy Organization’s Specialty and Training Council conducted a survey of World Allergy Organization (WAO) member societies to obtain information about the status of the specialty of allergy worldwide. Responses were received from 33 countries, representing a population of 1.39 billion people, of whom it was estimated that 22% may suffer from some form of allergic disease. Allergy was reported by 23 respondents to be a certified or accredited specialty in their country, and the number of certified allergists per head of population ranged from 1:25 million to 1:16,000. Allergists were ranked as the fifth most likely clinicians to see cases of allergic asthma, third most likely to see allergic rhinitis, and fourth most likely to see eczema or sinusitis. Nine countries only reported that children with allergic diseases would be seen by a pediatrician with appropriate training. The survey results highlight a pressing need for the development of allergy services worldwide.

Background Skin patch test is the gold standard method in diagnosing contact allergy. Although used for more than 100 years, the patch test procedure is performed with variability around the world. A number of factors can influence the test results, namely the quality of reagents used, the timing of the application, the patch test series (allergens/haptens) that have been used for testing, the appropriate interpretation of the skin reactions or the evaluation of the patient’s benefit. Methods We performed an Internet –based survey with 38 questions covering the educational background of respondents, patch test methods and interpretation. The questionnaire was distributed among all representatives of national member societies of the World Allergy Organization (WAO), and the WAO Junior Members Group. Results One hundred sixty-nine completed surveys were received from 47 countries. The majority of participants had more than 5 years of clinical practice (61 %) and routinely carried out patch tests (70 %). Both allergists and dermatologists were responsible for carrying out the patch tests. We could observe the use of many different guidelines regardless the geographical distribution. The use of home-made preparations was indicated by 47 % of participants and 73 % of the respondents performed 2 or 3 readings. Most of the responders indicated having patients with adverse reactions, including erythroderma (12 %); however, only 30 % of members completed a consent form before conducting the patch test. Discussion The heterogeneity of patch test practices may be influenced by the level of awareness of clinical guidelines, different training backgrounds, accessibility to various types of devices, the patch test series (allergens/haptens) used for testing, type of clinical practice (public or private practice, clinical or research-based institution), infrastructure availability, financial/commercial implications and regulations among others. Conclusion There is a lack of a worldwide homogeneity of patch test procedures, and this raises concerns about the need for standardization and harmonization of this important diagnostic procedure.

The prevalence of diseases such as allergic asthma and rhinitis continues to increase in the United States, affecting millions of people. It is well-established that allergy contributes to the pathogenesis of most asthma, especially in children and young adults. Despite current therapy (eg, inhaled corticosteroids, anti-leukotrienes, and bronchodilators), patients with moderate to severe asthma remain symptomatic and experience frequent exacerbations of disease requiring oral corticosteroids, emergency department treatments, and hospitalizations. Allergic diseases are traditionally referred to as immediate or type 1 hypersensitivity reactions , with IgE as a critical factor. IgE is involved in allergic inflammation, especially in early-phase response, but it may also be involved in the late-phase allergic response. A direct correlation between serum IgE levels and asthma exists. As logarithm IgE values increase, asthma prevalence increases linearly, even in patients who are categorized as having nonallergic asthma. In addition, there is a significant, although low association in allergic rhinitis with IgE levels and positive skin test reactivity to pollens. Recent advances in our understanding of the role of IgE in allergic inflammation have led to the development of a monoclonal antibody to IgE that reduces IgE levels, thereby reducing allergic inflammation. This review aims to provide an overview of the basic science of the IgE molecule and the clinical efficacy of anti-IgE therapy in allergic and asthmatic diseases.

The hypereosinophilic syndrome, although uncommon, is difficult to treat, and the treatment has substantial toxic effects. This proof-of concept trial shows that treatment of patients with the hypereosinophilic syndrome with an anti–interleukin-5 monoclonal antibody, mepolizumab, improves clinical and laboratory outcomes. This proof-of concept trial shows that treatment of patients with the hypereosinophilic syndrome with an anti–interleukin-5 monoclonal antibody, mepolizumab, improves clinical and laboratory outcomes. The hypereosinophilic syndrome consists of several heterogeneous disorders characterized by sustained blood eosinophilia and eosinophil-related end-organ damage, with no identifiable cause, such as parasitic infection. 1 The objective of treatment is long-term reduction of blood and tissue eosinophil levels to prevent end-organ damage and thromboembolic events. Except for the myeloproliferative variant of the hypereosinophilic syndrome (associated with the Fip1-like 1–platelet-derived growth factor receptor α fusion gene [ FIP1L1–PDGFRA ]), for which imatinib mesylate is considered first-line therapy, current management is based on long-term systemic corticosteroids. 1 – 4 Eosinophil development from hematopoietic progenitors is regulated mainly by interleukin-5, 5 which has a selective role . . .

ABSTRACT Background: Histamine receptor activation and degranulation of mast cells are the mechanisms by which the ocular itching, hyperemia, chemosis, eyelid swelling, and tearing of seasonal allergic conjunctivitis are induced. Some of the topical solutions available as anti-allergy therapies are intended to interfere with these mechanisms, and the body of research regarding the capabilities of these therapeutic molecules continues to expand. Objective: To review the currently available literature regarding one topical ophthalmic anti-allergy agent, olopatadine (Patanol*), and its anti-histaminic and mast cell stabilizing actions, both in pre-clinical and clinical settings. *Patanol is a registered trade name of Alcon Laboratories Inc, Fort Worth, TX, USA Design and methods: Relevant research of laboratory, animal model, and clinical trial studies performed using olopatadine was reviewed. MEDLINE literature searches were conducted and supplemented by additional reports which furthered relevant discussion or were necessary to verify the information resulting from original searches. Results: Olopatadine demonstrates unique properties both pre-clinically and clinically which differentiate it from other therapeutic molecules in its class of dual action mast cell stabilizer/anti-histamine. Its non-perturbation of cell membranes, human conjunctival mast cell stabilization in vivo and in vitro, and superior efficacy as compared to other topical anti-allergic medications including mast cell stabilizers, anti-histamines, and dual action agents, all contribute to olopatadine's profile. Conclusions: Peer-reviewed literature suggests that olopatadine is clinically superior to the other anti-allergic molecules because of its strong anti-histaminic qualities and its unique ocular mast cell stabilizing properties.

CD23 is the low-affinity Fc receptor for IgE. When expressed on B cells, CD23 appears to play a role in regulation of IgE synthesis. Polymorphisms within FCER2, the gene encoding CD23, have been associated with atopy, increased risk of exacerbations in patients with asthma, and high serum IgE levels. A single-nucleotide polymorphism (rs2228137) present in exon 4 of FCER2 encodes a nonsynonymous amino acid change (R62W) and is the subject of the present analysis. Human B cell stable transfectants were established to characterize the functional relevance of the R62W SNP. We demonstrate that CD23b-R62W-expressing human B cells bind IgE with greater affinity than wild-type cells and display differences in kinetics of CD23-mediated ERK1/2 activation that may be responsible for the increased levels of Egr-1 mRNA observed after stimulation through CD23. Finally, the R62W SNP seems to alter the tertiary or quaternary structure of CD23 because in the absence of N-glycosylation the CD23b-R62W-expressing cells appear to be less sensitive to endogenous proteases. These observations may have implications in mechanisms responsible for the atopic phenotypes observed in patients with asthma who possess this genotype.

Immunoglobulin E (IgE) plays a critical role in the allergic inflammatory process in diseases such as allergic rhinitis. Cross-linking IgE bound to its receptor on cells by multivalent allergens initiates a chain of events resulting in allergic immune responses. Mast cells and basophils are involved in the early, immediate response, which is marked by cellular degranulation and the release of proinflammatory mediators, including histamine. Antigen-presenting cells are also activated by allergen-loaded IgE, resulting in immunomodulation of T-cell responses. The IgE molecule binds to two types of receptors, the high-affinity (Fc epsilonRI) and low-affinity (Fc epsilonRII or CD23) receptors, that have differing properties important in mediating allergen-induced responses. New therapies targeting the IgE molecule reduce allergen-stimulated immune responses and improve the clinical symptoms in subjects with allergic rhinitis. Understanding the role of the IgE molecule is necessary to appreciate the development and use of novel therapies targeting its actions.