Clinical and pathologic perspectives on aspirin sensitivity and asthma

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Presentation transcript:

Clinical and pathologic perspectives on aspirin sensitivity and asthma Donald D. Stevenson, MD, Andrew Szczeklik, MD Journal of Allergy and Clinical Immunology Volume 118, Issue 4, Pages 773-786 (October 2006) DOI: 10.1016/j.jaci.2006.07.024 Copyright © 2006 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 1 Pathogenesis of AERD. Presumably, a damaging stimulus of respiratory epithelial cells initiates bone marrow formation of mast cell progenitor cells and eosinophils. In AERD these cells are the major contributors to local inflammation. Density and polymorphism of EP2 receptors, as well as cell-activating receptors, are not shown. Chemotaxis of new mast cell progenitor cells and eosinophils from bone marrow perpetuates the disease. AA, Arachidonic acid; ECP, eosinophil cationic protein; MBP, major basic protein. Journal of Allergy and Clinical Immunology 2006 118, 773-786DOI: (10.1016/j.jaci.2006.07.024) Copyright © 2006 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 2 Aspirin or NSAIDs induced respiratory reactions. Aspirin and NSAIDs inhibit COX-1, thus depriving mast cells and eosinophils of PGE2 to block the ongoing synthesis of LTs. Alteration in function of PGE2 receptors (particularly EP2) might contribute to the inability of PGE2 to sustain the blockade. From mast cells, PGD2 is oversynthesized, and histamine and tryptase are released during reactions. Eosinophil cationic protein (ECP) and major basic protein (MBP) are released from eosinophils. AA, Arachidonic acid. Journal of Allergy and Clinical Immunology 2006 118, 773-786DOI: (10.1016/j.jaci.2006.07.024) Copyright © 2006 American Academy of Allergy, Asthma and Immunology Terms and Conditions

Fig 3 Aspirin desensitization. After aspirin disables COX-1 and COX-2, inflammatory cells are unable to synthesize prostanoids, including the proinflammatory PGD2 and the anti-inflammatory PGE2. Histamine and tryptase are no longer released from mast cells. Eosinophils stop releasing toxic molecules. CysLT receptors are underexpressed after aspirin treatment, and it is likely that intracellular transcription factors are also inhibited by aspirin. Journal of Allergy and Clinical Immunology 2006 118, 773-786DOI: (10.1016/j.jaci.2006.07.024) Copyright © 2006 American Academy of Allergy, Asthma and Immunology Terms and Conditions