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. 2023 Nov 1;5(4):100282.
doi: 10.1016/j.opresp.2023.100282. eCollection 2023 Oct-Dec.

[Unmet Needs in Severe Allergic Asthma]

[Article in Spanish]
Julio Delgado  1 , Ana Navarro  1 , Francisco Javier Álvarez-Gutiérrez  2 , Carolina Cisneros  3 , Javier Domínguez-Ortega  4
Affiliations

[Unmet Needs in Severe Allergic Asthma]

[Article in Spanish]
Julio Delgado et al. Open Respir Arch. .

Abstract
in English, Spanish

Severe asthma affects 3%-10% of the world's population, according to estimates by the Global Initiative for ASTHMA (GINA). Allergic asthma is one of the most common phenotypes of severe asthma and it is characterized by allergen-induced type 2 inflammation in which immunoglobulin E (IgE) is a key mediator, making it an important therapeutic target. The introduction of targeted biological therapies or treatments has entered the management for severe asthma in the era of precision medicine, and the goal of treatment is clinical remission of the disease. There is a significant percentage of patients with severe allergic asthma who do not respond to treatments and whose symptoms are not controlled. In this paper, a group of experts in the management of severe allergic asthma reviewed and evaluated the most relevant evidence regarding the pathophysiology and phenotypes of severe allergic asthma, the role of IgE in allergic inflammation, allergen identification, techniques, biomarkers and diagnostic challenges, available treatments and strategies for disease management, with a special focus on biological treatments. From this review, recommendations were developed and validated through a Delphi consensus process with the aim of offering improvements in the management of severe allergic asthma to the professionals involved and identifying the unmet needs in the management of this pathology.

El asma grave afecta del 3 al 10% de la población mundial, según estimaciones de la Iniciativa Global para el ASMA (GINA). El asma alérgica es uno de los fenotipos más comunes del asma grave y se caracteriza por una inflamación de tipo 2 provocada por alérgenos y en el que la inmunoglobulina E (IgE) es una mediadora clave, lo que la ha convertido en una diana terapéutica importante. La introducción de las terapias o de los tratamientos biológicos dirigidos ha supuesto la entrada del manejo del asma grave en la era de la medicina de precisión y que el objetivo del tratamiento aspirase a la remisión clínica de la enfermedad. Existe un porcentaje importante de pacientes con asma alérgica grave que no responden a los tratamientos y cuyos síntomas no están controlados. En este documento, un grupo de expertos en el manejo del asma alérgica grave ha revisado y evaluado la evidencia más relevante relativa a la fisiopatología y a los fenotipos del asma grave alérgica, la función de la IgE en la inflamación alérgica, la identificación de alérgenos, las técnicas, biomarcadores y retos diagnósticos y los tratamientos y estrategias disponibles para el manejo de la enfermedad, con un especial foco en los tratamientos biológicos. A partir de esta revisión se han desarrollado unas recomendaciones que han sido validadas a través de un proceso de consenso Delphi con el objetivo de ofrecer mejoras en el manejo del asma alérgica grave a los profesionales implicados e identificar las necesidades no cubiertas en el manejo de esta patología.

Keywords: Allergens; Biomarkers; IgE; Omalizumab; Severe allergic asthma; Treatments.

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References

    1. Froidure A., Mouthuy J., Durham S.R., Chanez P., Sibille Y., Pilette C. Asthma phenotypes and IgE responses. Eur Respir J. 2016;47:304–319. doi: 10.1183/13993003.01824-2014. - DOI - PubMed
    1. Backman H., Raisanen P., Hedman L., Stridsman C., Andersson M., Lindberg A., et al. Increased prevalence of allergic asthma from 1996 to 2006 and further to 2016-results from three population surveys. Clin Exp Allergy. 2017;47:1426–1435. doi: 10.1111/cea.12963. - DOI - PubMed
    1. Moore W.C., Bleecker E.R., Curran-Everett D., Erzurum S.C., Ameredes B.T., Bacharier L., et al. Characterization of the severe asthma phenotype by the National Heart, Lung, and Blood Institute's Severe Asthma Research Program. J Allergy Clin Immunol. 2007;119:405–413. doi: 10.1016/j.jaci.2006.11.639. - DOI - PMC - PubMed
    1. Fitch K., Bernstein S.J., Aguilar M.D., Burnand B., Lacalle J.R., Lazaro P., et al. RAND Corporation; Santa Monica, CA: 2001. The RAND/UCLA Appropriateness Method User's Manual. Disponible en: https://www.rand.org/pubs/monograph_reports/MR1269.html. Also available in print form.
    1. Kraft S., Kinet J.P. New developments in FcepsilonRI regulation, function and inhibition. Nat Rev Immunol. 2007;7:365–378. doi: 10.1038/nri2072. - DOI - PubMed

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