Abstract
Aspirin-induced asthma (AIA) is a well-defined clinical syndrome that affects about 10% of adult asthmatics and in which aspirin and several other non-steroidal anti-inflammatory drugs (NSAID) precipitate asthmatic reactions1-4. Although the onset of symptoms before puberty or after the age of 60 has been well documented, in most patients the first symptoms appear during the third or fourth decade of life. Typically, the patient experiences intense vasomotor rhinitis characterized by intermittent and profuse watery rhinorrhoea. Over a period of months or years, chronic nasal congestion appears and physical examination reveals nasal polyps. Bronchial asthma and intolerance to aspirin develop subsequently. The intolerance presents as a unique picture: within an hour after ingestion of aspirin an acute asthma attack develops, often accompanied by rhinorrhoea, conjunctival irritation and scarlet flushing of the head and neck. Aspirin is a common precipitating factor of life-threatening attacks of asthma5; in a recent large survey, 25% of asthmatic patients requiring emergency mechanical ventilation were found to be aspirin intolerant6.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Samter M, Beers RF. Intolerance to aspirin. Clinical studies and consideration of its pathogenesis. Ann Intern Med. 1968; 68: 975–83.
Stevenson DD. Diagnosis, prevention and treatment of adverse reactions to aspirin and nonsteroidal anti-inflammatory drugs. J Allergy Clin Immunol. 1984; 74: 617–22.
Szczeklik A. Aspirin-induced asthma. In: Vane JR, Botting RM, editors. Aspirin and other salicylates. London: Chapman and Hall Medical, 1992: 548–75.
Szczeklik A. Mechanism of aspirin-induced asthma. Allergy. 1997; 52: 613–19.
Picado C, Castillo JA, Montserrat JM, Augusti-Vidal A. Aspirin-intolerance as a precipitating factor of life-threatening attacks of asthma requiring mechanical ventilation. Eur Resp J. 1989; 2: 127–9.
Marquette CH, Saulnier F, Leroy O, et al. Long-term prognosis for near-fatal asthma. A 6-year follow-up study of 145 asthmatic patients who underwent mechanical ventilation for near-fatal attack of asthma. Am Rev Resp Dis. 1992; 146: 76–81.
Szczeklik A, Schmitz-Schumann M, Nizankowska E, Milewski M, Roehlig F, Virchow C. Altered distribution of IgG subclasses in aspirin-induced asthma: high IgG4, low IgG1. Clin Exp Allergy. 1992; 22: 283–7.
Szczeklik A, Nizankowska E, Serafin A, Dyczek A, Duplaga M, Musial J. Autoimmune phenomena in bronchial asthma with special reference to aspirin intolerance. Am J Resp Crit Care Med. 1995; 152: 1753–6.
Lasalle P, Delneste Y, Gosset P, Grass-Masse H, Wallaert B, Tonne] AB T and B cell immune response to a 55-kDa endothelial cell-derived antigen in severe asthma. Eur J Immunol. 1993; 23. 796–803.
Szczeklik A, Musial J, Pulka G. Autoimmune vasculitis and aortic stenosis in aspirin-induced asthma. Allergy. 1997; 52: 352–4.
Bochenek G. Nizankowska E, Szczeklik A. Atopy trait in hypersensitivity to nonsteroidal anti-inflammatory drugs. Allergy. 1996; 51: 16–23.
Dekker JW, Nizankowska E, Schmitz-Schumann M, et al. Aspirin-induced asthma and HLA-DRBI and HLA-DPBI genotypes. Clin Exp Allergy. 1997; 27: 574–7.
Settipane RA, Schrank PJ, Simon RA, Mathison DA, Christiansen SC, Stevenson DD. Prevalence of cross-sensitivity with acetaminophen in aspirin-sensitive asthmatic subjects. J Allergy Clin Immunol. 1995; 96: 480–5.
Virchow Ch, Szczeklik A, Bianco S, et al. Intolerance to tartrazine in aspirin-induced asthma: results of a multicenter study. Respiration. 1988; 53: 20–3.
Szczeklik A. The cyclooxygenase theory of aspirin-induced asthma. Eur Resp J. 1990; 3: 588–93.
Vane JR. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs. Nature. 1971; 231: 232–4.
Szczeklik A, Gryglewski RJ, Czerniawska-Mysik G. Clinical patterns of hypersensitivity to nonsteroidal antiinflammatory drugs and their pathogenesis J Allergy Clin Immunol. 1977; 60: 276–84.
Szczeklik A, Gryglewski RJ, Czerniawska-Mysik G. Relationship of inhibition of prostaglandin biosynthesis by analgesics to asthma attacks in aspirin-sensitive patients. BMJ. 1975; 1:67–9.
Stevenson DD, Lewis RA. Proposed mechanisms of aspirin sensitivity reactions. J Allergy Clin Immunol. 1987; 80: 788–90.
Lee TH. Mechanism of aspirin sensitivity. Am Rev Resp Dis. 1992: 145: 34–6.
Bazan N, Botting J, Vane JR. New targets in inflammation. Inhibitors of COX-2 or adhesion molecules. Dordrecht: Kluwer and William Harvey Press, 1996.
Bianco S, Robuschi M, Petrigni G, et al. Efficacy and tolerability of nimesulide in asthmatic patients intolerant to aspirin. Drugs. 1993; 46 (suppl. 1): 115–20.
Busse WW. The role of leukotrienes in asthma and allergic rhinitis. Clin Exp Allergy. 1996; 26: 868–79.
Sampson AP. The leukotrienes: Mediators of chronic inflammation in asthma. Clin Exp Allergy. 1996; 26: 995–1004.
Smith CM, Hawksworth RJ, Thien FC, Christie PE, Lee TH. Urinary leukotriene E4 in bronchial asthma. Eur Resp J. 1992; 5: 693–9.
Christie PE, Tagari P, Ford-Hutchinson AW, Charlesson S, Chee P, Arm JP, Lee TH Urinary leukotriene E4 concentrations increase after aspirin challenge in aspirin-sensitive asthmatic subjects. Am Rev Resp Dis. 1991; 143: 1025–9.
Kumlin M, Dahlén B, Bjorck T, Zetterstrom O, Granstrom E, Dahlén SE. Urinary excretion of leukotriene E4 and 11-dehydro-thromboxane B2 in response to provocations with allergen, aspirin, leukotriene D4 and histamine in asthmatics. Am Rev Resp Dis. 1992; 146: 96–103.
Sladek K, Szczeklik A. Cysteinyl leukotrienes overproduction and mast cell activation in aspirin-provoked bronchospasm in asthma. Eur Resp J. 1993; 6: 391–9.
Ortolani C, Mirone C, Fontana A, et al. Study of mediators of anaphylaxis in nasal wash fluids after aspirin and sodium metabisulfite nasal provocation in intolerant rhinitic patients. Ann Allergy. 1987; 59: 106–12.
Ferreri NR, Howland WC, Stevenson DD, Spiegelberg HL. Release of leukotrienes, prostaglandins and histamine into nasal secretions of aspirin-sensitive asthmatic during reaction to aspirin. Am Rev Resp Dis. 1988; 137: 847–54.
Picado C, Ramis I, Rosello J, et al. Release of peptido-leukotrienes into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients. Am Rev Resp Dis. 1992; 145: 65–9.
Kowalski ML, Sliwinska-Kowalska M, et al. Nasal secretions in response to acetylsalicylic acid. J Allergy Clin Immunol. 1993; 91: 580–98.
Kowalski ML, Grzegorczyk J, Wojciechowska B, Pomatowska M. Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA-sensitive patients. Clin Exp Allergy. 1996; 26: 807–14.
Fischer AR, Rosenberg MA, Lilly CM, et al. Direct evidence for a role of the mast cell in the nasal response to aspirin in aspirin-sensitive asthma. J Allergy Clin Immunol. 1994; 94: 1046–56.
Wong D-Y, Smitz J, Clement P. Prostaglandin D2 measurement in nasal secretions is not a reliable marker for mast cell activation in atopic patients. Clin Exp Allergy. 1995; 25: 1228–34.
Szczeklik A, Sladek K, Dworski R, et al. Bronchial aspirin challenge causes specific eicosanoid response in aspirin sensitive asthmatics. Am J Resp Crit Care Med. 1996; 154: 1608–14.
Warren MS, Sloan SJ, Westcott JY, Hamilos D, Wenzel SE. LTE4 increases in bronchoalveolar lavage fluid (BALF) of aspirin-intolerant asthmatics (AIA) after instillation of indomethacin. J Allergy Clin Immunol. 1995; 95: 170.
Sampson AP, Coburn AS, Sladek K, et al. Profound overexpression of leukotriene C4 synthase in aspirin-intolerant asthmatic bronchial biopsies. Int Arch Allergy Immunol. 1977; 113: 355–7.
Nasser SMS, Pfister R, Christie PE, et al. Inflammatory cell populations in bronchial biopsies from aspirin-sensitive asthmatic subjects. Am J Resp Crit Care Med. 1996; 153: 90–6.
Christie PE, Smith CM, Lee TH. The potent and selective sulfidopeptide leukotriene antagonist, SK&F 104353, inhibits aspirin-induced asthma. Am Rev Resp Dis. 1991; 144: 957–8.
Dahlén B, Margolskee DJ, Zetterstrom O, Dahlén S-E. Effect of the leukotriene receptor antagonist MK-0679 on baseline pulmonary function in aspirin sensitive asthmatic subjects. Thorax. 1993; 48: 1205–10.
Yamamoto H, Nagata M, Kuramitsu K, et al. Inhibition of analgesic-induced asthma by leukotriene receptor antagonist ONO-1078. Am J Resp Crit Care Med. 1994; 150: 254–7.
Szczeklik A, Serwonska M. Inhibition of idiosyncratic reactions to aspirin in asthmatic patients by clemastine. Thorax. 1979; 34: 654–7.
Philips GD, Foord R, Holgate ST. Inhaled lysine-aspirin as a bronchoprovocation procedure in aspirin-sensitive asthma: Its repeatability absence of a late-phase reaction and the role of histamine. J Allergy Clin Immunol. 1989; 84: 232–41.
Dahlén S-E, Niiankowska E, Dahlén B, et al. The Swedish-Polish treatment study with the 5-lipoxygenase inhibitor Zileuton in aspirin-intolerant asthmatics. Am J Resp Crit Care Med. 1995; 151: A376.
Kuna P, Malmström K, Dahlén S-E, et al. Montelukast (MK-0476), a cys-LT1 receptor antagonist, improves asthma control in aspirin-intolerant asthmatic patients. Am J Resp Crit Care Med. 1997; 155: A975.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1998 Springer Science+Business Media Dordrecht
About this chapter
Cite this chapter
Szczeklik, A., Sanak, M. (1998). Role of leukotrienes in aspirin-induced asthma. In: Rodger, I., Botting, J., Dahlén, SE. (eds) Leukotrienes. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4880-1_9
Download citation
DOI: https://doi.org/10.1007/978-94-011-4880-1_9
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-6045-5
Online ISBN: 978-94-011-4880-1
eBook Packages: Springer Book Archive