Cargando…

Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?

Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in a...

Descripción completa

Detalles Bibliográficos
Autores principales: Van Broeck, Dorien, Steelant, Brecht, Scadding, Glenis, Hellings, Peter W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10130434/
https://www.ncbi.nlm.nih.gov/pubmed/37123562
http://dx.doi.org/10.3389/falgy.2023.1080951
_version_ 1785030956782977024
author Van Broeck, Dorien
Steelant, Brecht
Scadding, Glenis
Hellings, Peter W.
author_facet Van Broeck, Dorien
Steelant, Brecht
Scadding, Glenis
Hellings, Peter W.
author_sort Van Broeck, Dorien
collection PubMed
description Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in associated asthma exacerbations, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries. Unknown influences cause polyp epithelium to release alarmins, such as IL-33 and TSLP. These cytokines activate lymphoid cells, both Th2 and ILC2, to release cytokines such as IL5, IL4 and IL13, resulting in complex type 2 inflammation involving mast cells, eosinophils and platelets. Arachidonic acid released from such cells is metabolized into mediators. N-ERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. Patients with N-ERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives. Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with N-ERD. The most important strategies for treating N-ERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. N-ERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential. This review provides an overview on aspirin desensitization and biologics in N-ERD and might help in decision making from both the perspective of the physician and patient. Patient characteristics, safety, efficacy, health care costs, but also patient preferences are all factors to take into account when it comes to a choice between biologics or aspirin desensitization.
format Online
Article
Text
id pubmed-10130434
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-101304342023-04-27 Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)? Van Broeck, Dorien Steelant, Brecht Scadding, Glenis Hellings, Peter W. Front Allergy Allergy Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin/NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. N-ERD results in associated asthma exacerbations, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries. Unknown influences cause polyp epithelium to release alarmins, such as IL-33 and TSLP. These cytokines activate lymphoid cells, both Th2 and ILC2, to release cytokines such as IL5, IL4 and IL13, resulting in complex type 2 inflammation involving mast cells, eosinophils and platelets. Arachidonic acid released from such cells is metabolized into mediators. N-ERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. Patients with N-ERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives. Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with N-ERD. The most important strategies for treating N-ERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. N-ERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential. This review provides an overview on aspirin desensitization and biologics in N-ERD and might help in decision making from both the perspective of the physician and patient. Patient characteristics, safety, efficacy, health care costs, but also patient preferences are all factors to take into account when it comes to a choice between biologics or aspirin desensitization. Frontiers Media S.A. 2023-04-12 /pmc/articles/PMC10130434/ /pubmed/37123562 http://dx.doi.org/10.3389/falgy.2023.1080951 Text en © 2023 Van Broeck, Steelant, Scadding and Hellings. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Allergy
Van Broeck, Dorien
Steelant, Brecht
Scadding, Glenis
Hellings, Peter W.
Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title_full Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title_fullStr Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title_full_unstemmed Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title_short Monoclonal antibody or aspirin desensitization in NSAID-exacerbated respiratory disease (N-ERD)?
title_sort monoclonal antibody or aspirin desensitization in nsaid-exacerbated respiratory disease (n-erd)?
topic Allergy
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10130434/
https://www.ncbi.nlm.nih.gov/pubmed/37123562
http://dx.doi.org/10.3389/falgy.2023.1080951
work_keys_str_mv AT vanbroeckdorien monoclonalantibodyoraspirindesensitizationinnsaidexacerbatedrespiratorydiseasenerd
AT steelantbrecht monoclonalantibodyoraspirindesensitizationinnsaidexacerbatedrespiratorydiseasenerd
AT scaddingglenis monoclonalantibodyoraspirindesensitizationinnsaidexacerbatedrespiratorydiseasenerd
AT hellingspeterw monoclonalantibodyoraspirindesensitizationinnsaidexacerbatedrespiratorydiseasenerd