title: Aspirin and asthma.
abstract: Aspirin is not only one of the best-documented medicines in the world, but also one of the most frequently used drugs of all times. In addition to its role as an analgesic, aspirin is being increasingly used in the prophylaxis of ischemic heart disease and strokes. The prevalence of aspirin intolerance is around 5 to 6%. Up to 20% of the asthmatic population is sensitive to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) and present with a triad of rhinitis, sinusitis, and asthma when exposed to the offending drugs. This syndrome is referred to as aspirin-induced asthma (AIA). The pathogenesis of AIA has implicated both the lipoxygenase (LO) and the cyclooxygenase (COX) pathways. By inhibiting the COX pathway, aspirin diverts arachidonic acid metabolites to the LO pathway. This also leads to a decrease in the levels of prostaglandin (PG) E(2), the anti-inflammatory PG, along with an increase in the synthesis of cysteinyl leukotrienes (LTs). Evidence suggests that patients with AIA have increased activity of LTC(4) synthase, the rate-limiting enzyme in the cysteinyl LT synthesis, in their bronchial biopsy specimens, thereby tilting the balance in favor of inflammation. LT-modifying drugs are effective in blocking the bronchoconstriction provoked by aspirin and are used in the treatment of this condition. Aspirin desensitization has a role in the management of AIA, especially in patients who need prophylaxis from thromboembolic diseases, myocardial infarction, and stroke. This review covers the latest understanding of pathogenesis, clinical features, and management of AIA.
authors.affiliation: Department of Respiratory Cell and Molecular Biology, University of Southampton, Southampton General Hospital, Southampton, UK. ksb@soton.ac.uk
authors.forename: K S
authors.initials: KS
authors.lastname: Babu
authors.forename: S S
authors.initials: SS
authors.lastname: Salvi
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001095:Arachidonic Acids / Q000378:metabolism; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced / Q000503:physiopathology* / Q000517:prevention & control; D016535:Bronchial Hyperreactivity / Q000517:prevention & control; D016861:Cyclooxygenase Inhibitors / Q000009:adverse effects; D003888:Desensitization, Immunologic; D015232:Dinoprostone / Q000037:antagonists & inhibitors; D004342:Drug Hypersensitivity / Q000209:etiology*; D005982:Glutathione Transferase / Q000187:drug effects; D006801:Humans; D020024:Leukotriene Antagonists; D017998:Leukotriene D4 / Q000096:biosynthesis; D008084:Lipoxygenase / Q000378:metabolism; D012220:Rhinitis / Q000139:chemically induced; D012852:Sinusitis / Q000139:chemically induced
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D020024:Leukotriene Antagonists; D017998:Leukotriene D4; D008084:Lipoxygenase; D005982:Glutathione Transferase; C041116:leukotriene-C4 synthase; D015232:Dinoprostone; D001241:Aspirin