title: [Physiopathology of aspirin intolerant asthma].
abstract: Aspirin-exacerbated respiratory disease (AERD) refers to the development of bronchoconstriction in individuals with asthma following the ingestion of aspirin. AERD affects up to 20 % of adults with asthma. At present, no reliable in vitro test is available to confirm the diagnosis. The confirmation of the diagnosis of AERD therefore depends on the response to challenge testing with aspirin. The pathogenesis of AERD is linked to abnormalities in arachidonic acid metabolism. Prior to exposure to aspirin, respiratory mucosal inflammation is the result of a cell infiltration, an overproduction of leukotrienes, prostaglandins D2, 5-oxo-eicosatetraenoic acid and an underproduction of lipoxins. After aspirin ingestion, patients with AERD synthesize excessive amounts of cysteinyl leukotrienes and prostaglandin metabolites involved in bronchoconstriction. New hypotheses concerning AERD pathogenesis have been added to the initial cyclooxygenase theory. These propose that AERD may be linked to the complement system, adenosine metabolism or angiotensin converting enzyme gene and IgE receptor gene polymorphisms.
authors.affiliation: Service de pneumologie, centre hospitalier Lyon-Sud, Lyon, France.
authors.forename: A
authors.initials: A
authors.lastname: Carsin
authors.forename: J
authors.initials: J
authors.lastname: Bienvenu
authors.forename: Y
authors.initials: Y
authors.lastname: Pacheco
authors.forename: G
authors.initials: G
authors.lastname: Devouassoux
mesh_terms: D001095:Arachidonic Acids / Q000378:metabolism; D055963:Asthma, Aspirin-Induced / Q000503:physiopathology*; D002352:Carrier Proteins / Q000235:genetics; D018925:Chemokines / Q000235:genetics; D003165:Complement System Proteins / Q000032:analysis; D037161:Galectins / Q000235:genetics / Q000378:metabolism; D006632:Histamine / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology; D015289:Leukotrienes / Q000378:metabolism; D044045:Lipoxins / Q000378:metabolism; D046228:Microarray Analysis; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D018919:Neovascularization, Physiologic; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D011110:Polymorphism, Genetic; D015230:Prostaglandin D2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D017455:Receptors, IgE / Q000235:genetics; D018047:Receptors, Purinergic P1 / Q000235:genetics; D020545:Respiratory Mucosa / Q000378:metabolism / Q000503:physiopathology; D053802:Tryptases / Q000378:metabolism
chemical_list: D001095:Arachidonic Acids; D002352:Carrier Proteins; D018925:Chemokines; D037161:Galectins; D015289:Leukotrienes; D044045:Lipoxins; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human; D012333:RNA, Messenger; D017455:Receptors, IgE; D018047:Receptors, Purinergic P1; C523496:galectin 10, human; D006632:Histamine; D003165:Complement System Proteins; D007703:Peptidyl-Dipeptidase A; D053802:Tryptases; D015230:Prostaglandin D2