| Autor: |
Stevens W; Division of Allergy-Immunology, Department of Medicine, Northwestern University Feinberg School of Medicine, 211 East Ontario Street, Suite 1000, Chicago, IL, 60611, USA. whitney-stevens@northwestern.edu., Buchheit K; Division of Rhematology, Immunology, and Allergy, Department of Medicine, Brigham and Women's Hospital/Harvard Medical School, 1 Jimmy Fund Way, Smith Building Room 638, Boston, MA, 02115, USA. kbuchheit@partners.org., Cahill KN; Division of Rhematology, Immunology, and Allergy, Department of Medicine, Brigham and Women's Hospital/Harvard Medical School, 1 Jimmy Fund Way, Smith Building Room 638, Boston, MA, 02115, USA. kncahill@partners.org. |
| Abstrakt: |
Aspirin-exacerbated diseases are important examples of drug hypersensitivities and include aspirin-exacerbated respiratory disease (AERD), aspirin- or non-steroidal anti-inflammatory drug (NSAID)-induced urticaria/angioedema, and aspirin- or NSAID-induced anaphylaxis. While each disease subtype may be distinguished by unique clinical features, the underlying mechanisms that contribute to these phenotypes are not fully understood. However, the inhibition of the cyclooxygenase-1 enzyme is thought to play a significant role. Additionally, eosinophils, mast cells, and their products, prostaglandins and leukotrienes, have been identified in the pathogenesis of AERD. Current diagnostic and treatment strategies for aspirin-exacerbated diseases remain limited, and continued research focusing on each of the unique hypersensitivity reactions to aspirin is essential. This will not only advance the understanding of these disease processes, but also lead to the subsequent development of novel therapeutics that patients who suffer from aspirin-induced reactions desperately need. |
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