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Aspirin-induced Asthma And Cyclooxygenases

R. J. Gryglewski
Published 1998 · Medicine

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Bronchial asthma, irrespective of its specific triggers (allergens, cold, physical exercise or aspirin), is by and large an inflammatory disease. High plasma levels of immunoglobulin E (lgE), if present, indicate its atopic aetiology. Activated T lymphocytes (Th2) release various cytokines which promote recruitment, activation and secretion of mast cells, eosinophils and macrophages in the airways. Activation of these cells is associated with local release of pro-inflammatory, bronchoconstrictor or cytotoxic agents such as interleukins, proteases, superoxide anion (02-), histamine, platelet activating factor (PAF) and a number of eicosanoids including sulphidopeptide-Ieukotrienes (LTC4-E4), leukotriene BiLTB4)' thromboxane A2 (TXA2), prostaglandins F 20t and DiPGF20t and PGD2). These mediators contribute to an increase in vascular permeability, oedema, migration of leukocytes to tissues, epithelial shedding, fibroblast proliferation, bronchoconstriction, hyperreactivity of bronchi, rhinorrhea, cough and wheezing. Endogenous anti-inflammatory g1ucocorticoids, 13 adrenergic tone and the bronchodilator prostaglandin E2 (PGE2) counterbalance the pro-inflammatory cascade in the airways. Nitric oxide (NO) plays an ambiguous role in inflammatory response; however, in the lung it acts in opposition to pneumotoxic lipids (PAF, LTC4-E4, TXA2), unless overproduction of NO, together with O2- yields toxic peroxynitrite (ONOO-). Although asthma is an inflammatory disease, asthmatic patients do not necessarily benefit from all types of anti-inflammatory drugs. Certainly, anti-inflammatory g1ucocorticoids applied either systemically or locally are the most powerful anti­ asthmatic drugs. Selective 13-adrenomimetics or stabilizers of mast cell and eosinophil membranes, such as cromoglycate disodium and nedocromil sodium, are also used in the therapy of asthma. However, for example, cyclosporine, an immunosuppressor of T lymphocytes, or antagonists of histamine HI receptors hold a modest position in anti-asthmatic therapy. PGE2 inhalations are not used for the treatment of asthma since they produce cough and retrosternal pain. Aspirin and other non-steroidal anti­ inflammatory drugs (NSAID) differentiate the adult population of asthmatic patients into three subgroups. Aspirin-tolerant asthma (ATA, 90% of patients), aspirin­ induced asthma (AlA, 10% of patients) and aspirin-relieved asthma (ARA, 0.3% of patients). It is evident that only a few patients with asthma benefit from the treatment with aspirin: in most patients aspirin does not influence the course of the disease. In 10% of patients aspirin elicits acute asthmatic attacks, starting with wheezing, obstruc­ tion of airflow, sometimes accompanied by rhinorrhea, urticaria, angioedema, coronary vasospasm and other vascular disturbances. This paradox of AlA patients will be the subject of this chapter.
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