Does aspirin therapy after desensitization still have a role in treatment of chronic rhinosinusitis with nasal polyposis in the era of biologics?
© 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature..
The prevalence of analgesic intolerance syndrome (AIS), internationally known as NSAID-exacerbated respiratory disease (NERD), is reported to be 0.5-5.7% in the general population. The disease often begins with nasal symptoms, which are later joined by chronic rhinosinusitis with nasal polyposis (CRSwNP), asthma, and respiratory hypersensitivity reactions following use of nonsteroidal anti-inflammatory drugs (NSAIDs). In the setting of chronic respiratory disease, the type 2 inflammatory endotype is predominant in approximately 80% of patients with CRSwNP, rendering biologics directed against interleukin (IL)-4, IL‑5, IL-13, and IgE of high clinical interest, particularly in patients with severe CRSwNP and NERD. NERD is often associated with CRSwNP and asthma. Patients with CRSwNP and NERD have been treated, among other therapies, with aspirin therapy after desensitization (ATAD). With the approval of monoclonal antibodies for CRSwNP and asthma, the question arises as to what extent ATAD, which is associated with undesirable side effects, is still useful in the treatment of CRSwNP. In this manuscript, the use of ATAD in CRSwNP patients is discussed from different medical and socioeconomic points of view, both alternatively to or in combination with monoclonal antibodies. Accordingly, both ATAD and biologics continue to play a supporting role in modern treatment of CRSwNP in NERD patients, and should be used judiciously to complement each other.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2024 |
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Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - year:2024 |
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Enthalten in: |
HNO - (2024) vom: 26. Feb. |
Sprache: |
Deutsch |
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Weiterer Titel: |
Hat die ASS-Desaktivierung in Zeiten von Biologika noch einen Stellenwert bei chronischer Rhinosinusitis mit nasaler Polyposis? |
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Beteiligte Personen: |
Klimek, F [VerfasserIn] |
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Links: |
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Themen: |
Aspirin deactivation |
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Anmerkungen: |
Date Revised 27.02.2024 published: Print-Electronic Citation Status Publisher |
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doi: |
10.1007/s00106-024-01431-0 |
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funding: |
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PPN (Katalog-ID): |
NLM368995194 |
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245 | 1 | 0 | |a Does aspirin therapy after desensitization still have a role in treatment of chronic rhinosinusitis with nasal polyposis in the era of biologics? |
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520 | |a The prevalence of analgesic intolerance syndrome (AIS), internationally known as NSAID-exacerbated respiratory disease (NERD), is reported to be 0.5-5.7% in the general population. The disease often begins with nasal symptoms, which are later joined by chronic rhinosinusitis with nasal polyposis (CRSwNP), asthma, and respiratory hypersensitivity reactions following use of nonsteroidal anti-inflammatory drugs (NSAIDs). In the setting of chronic respiratory disease, the type 2 inflammatory endotype is predominant in approximately 80% of patients with CRSwNP, rendering biologics directed against interleukin (IL)-4, IL‑5, IL-13, and IgE of high clinical interest, particularly in patients with severe CRSwNP and NERD. NERD is often associated with CRSwNP and asthma. Patients with CRSwNP and NERD have been treated, among other therapies, with aspirin therapy after desensitization (ATAD). With the approval of monoclonal antibodies for CRSwNP and asthma, the question arises as to what extent ATAD, which is associated with undesirable side effects, is still useful in the treatment of CRSwNP. In this manuscript, the use of ATAD in CRSwNP patients is discussed from different medical and socioeconomic points of view, both alternatively to or in combination with monoclonal antibodies. Accordingly, both ATAD and biologics continue to play a supporting role in modern treatment of CRSwNP in NERD patients, and should be used judiciously to complement each other | ||
650 | 4 | |a English Abstract | |
650 | 4 | |a Journal Article | |
650 | 4 | |a Review | |
650 | 4 | |a Aspirin deactivation | |
650 | 4 | |a Monoclonal antibodies | |
650 | 4 | |a NSAID-exacerbated respiratory disease | |
650 | 4 | |a Respiratory hypersensitivity | |
650 | 4 | |a Type 2 inflammation | |
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