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Aspirin-induced Asthma And Cyclooxygenases

R. 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.
This paper references
Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.
J. Vane (1971)
Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients.
A. Szczeklik (1975)
Corticosteroids inhibit prostaglandin release from perfused mesenteric blood vessels of rabbit and from perfused lungs of sensitized guinea pig.
R. Gryglewski (1975)
Aspirin-Sensitive Asthma: Its Relationship to Inhibition of Prostaglandin Biosynthesis
R. J. Gryglewski (1977)
Prostaglandins and thromboxanes.
B. Samuelsson (1978)
Elimination of bagassosis in Louisiana paper manufacturing plant workers
S. Lehrer (1978)
Hydrocortisone and airflow impairment in aspirin-induced asthma.
A. Szczeklik (1985)
[Aspirin-induced asthma].
A. Szczeklik (1986)
Is coronary arterial spasm part of the aspirin-induced asthma syndrome?
M. Habbab (1986)
Effects of inhibition of thromboxane A2 synthesis in aspirin-induced asthma.
A. Szczeklik (1987)
Intolerance to tartrazine in aspirin-induced asthma: results of a multicenter study.
C. Virchow (1988)
Aspirin‐induced asthma as a viral disease
A. Szczeklik (1988)
Airway responsiveness to histamine and leukotriene E4 in subjects with aspirin-induced asthma.
J. Arm (1989)
[Acute myocardial injury and repeated angina pectoris-like attacks in a young patient with Churg-Strauss syndrome].
N. Suzuki (1991)
Aspirin-sensitive asthma: significance of the cyclooxygenase-inhibiting and protein-binding properties of analgesic drugs.
W. R. Williams (1991)
Increased excretion of leukotriene E4 during aspirin-induced asthma.
H. Knapp (1992)
Tolerance to aspirin in aspirin-sensitive asthmatics. Methods of inducing the tolerance state and its influence on the course of asthma and rhinosinusitis.
M. Szmidt (1993)
[Immunohistological study of eosinophilic infiltration of nasal polyps in aspirin-induced asthma].
R. Yoshimi (1993)
Lipoxygenase inhibitor-provoked acute asthma in a patient with asthma relieved by aspirin.
S. Imokawa (1995)
[Examination on aspirin-induced asthma and hypersensitivity to steroids--a questionnaire to 850 asthma on hypersensitivity to non-steroidal anti-inflammatory drugs and hypersensitivity to steroids].
T. Enomoto (1995)
Autoimmune vasculitis preceding aspirin-induced asthma.
A. Szczeklik (1995)
Increased urinary excretion of the prostaglandin D2 metabolite 9 alpha, 11 beta-prostaglandin F2 after aspirin challenge supports mast cell activation in aspirin-induced airway obstruction.
S. O'Sullivan (1996)
Anti-leukotriene intervention: is there adequate information for clinical use in asthma?
P. Ind (1996)
Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma.
P. Sestini (1996)
Mast cell effector mechanisms.
S. Lane (1996)
Effect of endobronchial aspirin challenge on inflammatory cells in bronchial biopsy samples from aspirin-sensitive asthmatic subjects.
S. Nasser (1996)
Intolerance to nonsteroidal antiinflammatory drugs: results of controlled drug challenges in 98 patients.
J. Quiralte (1996)
Protective and bronchodilator effects of prostaglandin E and salbutamol in aspirin-induced asthma.
A. Szczeklik (1996)
Bronchial aspirin challenge causes specific eicosanoid response in aspirin-sensitive asthmatics.
A. Szczeklik (1996)
Leukotrienes in asthma. The potential therapeutic role of antileukotriene agents.
L. Smith (1996)

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