title: Platelets in patients with aspirin-exacerbated respiratory disease.
abstract: Aspirin-exacerbated respiratory disease (AERD) is a chronic inflammatory disease characterized clinically by the triad of asthma, nasal polyposis, and pathognomonic respiratory reactions after ingestion of aspirin. It is a distinct syndrome associated with eosinophilic infiltration of respiratory tissues and excessive production of cysteinyl leukotrienes. Despite the consistent clinical phenotype of the respiratory disease, the underlying pathogenesis of the disease remains unclear. In addition to their role in hemostasis, platelets have the capacity to influence the activation state and function of other immune cells during inflammation and to facilitate granulocyte recruitment into the tissues. Platelets also possess a repertoire of potent preformed mediators of inflammation that are released on activation and are a rich source of newly synthesized lipid mediators that alter vascular permeability and smooth muscle tone. Accordingly, platelet activity has been linked to diverse inflammatory diseases, including asthma. Both human and animal studies strongly suggest that platelet activity is uniquely associated with the pathophysiology of AERD. This article summarizes the evidence supporting an effector role for platelets in asthmatic patients in general and in patients with AERD in particular and considers the potential therapeutic implications.
authors.affiliation: Department of Medicine, Harvard Medical School, Boston, Mass; Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, Mass. Electronic address: tlaidlaw@partners.org.
authors.forename: Tanya M
authors.initials: TM
authors.lastname: Laidlaw
authors.affiliation: Department of Medicine, Harvard Medical School, Boston, Mass; Department of Pediatrics, Harvard Medical School, Boston, Mass; Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, Mass.
authors.forename: Joshua A
authors.initials: JA
authors.lastname: Boyce
mesh_terms: D000818:Animals; D001241:Aspirin / Q000276:immunology; D055963:Asthma, Aspirin-Induced / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D001792:Blood Platelets / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000627:therapeutic use*; D002465:Cell Movement; D002986:Clinical Trials as Topic; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D015870:Gene Expression; D006801:Humans; D015289:Leukotrienes / Q000096:biosynthesis; D010080:Oxazoles / Q000627:therapeutic use*; D010879:Piperazines / Q000627:therapeutic use*; D010972:Platelet Activating Factor / Q000235:genetics / Q000276:immunology; D015539:Platelet Activation; D000068799:Prasugrel Hydrochloride; D018077:Receptors, Leukotriene / Q000235:genetics / Q000276:immunology; D013876:Thiophenes / Q000627:therapeutic use*; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors / Q000096:biosynthesis
chemical_list: D019086:Bridged Bicyclo Compounds, Heterocyclic; D015289:Leukotrienes; D010080:Oxazoles; D010879:Piperazines; D010972:Platelet Activating Factor; D018077:Receptors, Leukotriene; D013876:Thiophenes; D013928:Thromboxane A2; C078904:ifetroban; D000068799:Prasugrel Hydrochloride; D001241:Aspirin
keywords: Platelet; aspirin-exacerbated respiratory disease; asthma; eosinophil; leukotriene; nasal polyp; prostaglandin; samter triad; thromboxane