Abstract
Aspirin intolerance syndrome is due to disturbances in the arachidonic acid metabolism implicating both the lipoxygenase and cyclooxygenase pathways. This results in imbalances of eicosanoid, leukotriene and prostaglandin synthesis. Thus, preinflammatory cysteinyl leukotrienes increase and antiinflammatory prostaglandins (PG) such as PGE2 decrease. Clinically, intolerance reactions to nonsteroidal antiinflammatory drugs (NSAIDs) can lead to different clinical manifestations; five phenotypes of the aspirin intolerance syndrome are listed in the ENDA classification. Aspirin-exacerbated respiratory disease (AERD) is the most common phenotype characterized by an eosinophil-dominated inflammatory disease of the airways that presents clinically with nasal polyps, chronic sinusitis and bronchial asthma. About 34 % of patients with aspirin-induced asthma and rhinosinusitis are thought to have AERD. Important biochemical findings in many AERD patients are increased basal leukotriene levels (at least in cell cultures) that excessively increase after intake of COX-1 inhibitors. Aspirin desensitization uses the repetitive application of aspirin to induce a tolerance to NSAIDs, especially COX-1 inhibitors. After a dose-increase phase reaching a threshold dose, a dose-continuation phase is performed. For application, the nasal, bronchial, oral and intravenous routes have been described. Aspirin desensitization has been proven to be efficacious and safe and was able to reduce the need for other medications in AERD patients.
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Acknowledgments
R. Dollner has received grant support from Phadia/Thermofisher and MEDA.
Oliver Pfaar has received research grants from ALK-Abello, Allergopharma, Stallergenes, HAL, Artu Biologicals, Allergy-Therapeutics/Bencard, Hartington, Lofarma, Novartis/LETI, GlaxoSmithKline, Essex-Pharma, Cytos, Curalogic, Roxall, Biomay, Thermo-Fisher and MEDA Pharma GmbH and/or has served as an advisor and on speakers’ bureaus for some of the aforementioned pharmaceutical companies. Oliver Pfaar has also received travel grants from HAL Allergy and Allergopharma and has served as a consultant for Bencard/Allergy-Therapeutics, Biotech Tools s.s., HAL Allergy, LETI, MEDA, Stallergenes and Novartis; Oliver Pfaar is also current chairman of the EAACI Interest Group Immunotherapy (IG IT) and current secretary of the ENT section of DGAKI.
Joaquim Mullol has been a member of national and international scientific advisory boards (consulting), received fees for lectures and received grant support for research projects from ALK-Abelló, Boehringer Ingelheim, Crucell, Esteve, FAES, GlaxoSmithKline, Hartington, Johnson & Johnson, MEDA, Merck, Sharp & Dohme, Novartis, Pierre Fabre, Sanofi-Aventis and the Uriach Group.
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Conflict of Interest
Ludger Klimek received honoraria for lecturing and performing clinical studies from ALK-Abello, Allergopharma, Artu-Biologicals, Bencard, Bionorica, Biomay, Boehringer Ingelheim and Cytos, and Dr. Pfleger from HAL, Hartington, GlaxoSmithKline, Leti, Lofarma, Novartis, MEDA, Merck Sharp & Dohme, Phadia/Thermofisher, Optima and Roxall.
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This article does not contain any studies with animal subjects performed by any of the authors. With regard to the authors’ research cited in this paper, all procedures were followed in accordance with the ethical standards of the responsible committee on human experimentation and with the Helsinki Declaration of 1975, as revised in 2000 and 2008.
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Klimek, L., Dollner, R., Pfaar, O. et al. Aspirin Desensitization: Useful Treatment for Chronic Rhinosinusitis with Nasal Polyps (CRSwNP) in Aspirin-Exacerbated Respiratory Disease (AERD)?. Curr Allergy Asthma Rep 14, 441 (2014). https://doi.org/10.1007/s11882-014-0441-9
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DOI: https://doi.org/10.1007/s11882-014-0441-9