Review and Feature Article
IgE-Mediated Multimorbidities in Allergic Asthma and the Potential for Omalizumab Therapy

https://doi.org/10.1016/j.jaip.2019.02.030Get rights and content
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Allergic asthma often coexists with different pathological conditions, called multimorbidities, that are mostly of allergic nature and share a common underlying inflammatory pathophysiological mechanism. Multimorbidities of allergic asthma may influence asthma control, its severity, and patients' response to treatment, and contribute to the overall socioeconomic burden of the disease. Immunoglobulin E (IgE) is known to play a central role in the pathogenesis of various allergic diseases, including asthma. Thus, IgE-mediated immunologic pathways present an attractive target for intervention in asthma and multimorbidities. In this review, we discuss the most frequently reported IgE-mediated multimorbidities in allergic asthma, including allergic rhinitis, rhinoconjunctivitis, atopic dermatitis, vernal keratoconjunctivitis, chronic rhinosinusitis with nasal polyps, food allergies, and allergic bronchopulmonary aspergillosis. Omalizumab is a recombinant humanized monoclonal antibody against IgE and has been in use to treat allergic asthma for more than a decade. We comprehensively review the clinical evidence for omalizumab in the treatment of the aforementioned multimorbidities in allergic asthma.

Key words

Omalizumab
Asthma
Multimorbidities
Treatment
Allergic rhinitis
Rhinoconjunctivitis
Chronic rhinosinusitis with nasal polyps
Vernal keratoconjunctivitis
Food allergies
Allergic bronchopulmonary aspergillosis

Abbreviations used

ABPA
Allergic bronchopulmonary aspergillosis
AD
Atopic dermatitis
AR
Allergic rhinitis
CRS
Chronic rhinosinusitis
CRSsNP
Chronic rhinosinusitis without nasal polyps
CRSwNP
Chronic rhinosinusitis with nasal polyps
CSU
Chronic spontaneous urticaria
MeDALL
Mechanisms of the Development of ALLergy program
OIT
Oral immunotherapy
SE
Staphylococcus aureus enterotoxin
Spl
Staphylococcus aureus–derived serine protease–like protein
Th2 cells
T-helper-2 cells
VKC
Vernal keratoconjunctivitis

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No funding was received for this work.

Conflicts of interest: M. Humbert reports personal fees from AstraZeneca, Novartis, Roche, Sanofi, and TEVA, during the conduct of the study; and reports grants and personal fees from GSK. J. Bousquet reports personal fees and other from Chiesi, Cipla, Hikma, Menarini, Mundipharma, Mylan, Novartis, Sanofi-Aventis, Takeda, Teva, and Uriach; and reports other from KYomed-INNOV, outside the submitted work. C. Bachert reports advisory board and presentation fees received from Sanofi, Novartis, Astra-Zeneca, GSK, ALK, Stallergenes, ASIT Biotech, and Actobiotics. O. Palomares received lecture fees from Novartis, Sanofi-Genzyme, AstraZeneca, Amgen, Inmunotek S.L., Allergic Therapeutics, and Stallergenes; participated in advisory boards from Novartis and Sanofi-Genzyme; and received research grants from Novartis, ImmunoTek, and MINECO. P. Pfister, I. Kottakis, and X. Jaumont are employees of Novartis Pharma AG. S. F. Thomsen has been a paid speaker, served on advisory boards, been an investigator, and received research grants from Novartis. N. G. Papadopoulos has received research support from Gerolymatos, Menarini, Nutricia, and Vian; speaker fees from AstraZeneca, Boehringer Ingelheim, HAL, Menarini, MSD, Mylan, Novartis, and Nutricia; participated in advisory boards from ASIT, AZ, Biomay, Chiesi, HAL, Menarini, Mylan, Novartis, Nutricia, and Wockhardt; serves as the president of REG, CAP; is a board member of GA2LEN, ResViNET; and is a committee member of European Academy of Allergy and Clinical Immunology, World Allergy Organization.