Zusammenfassung
Überempfindlichkeitsreaktionen auf nichtsteroidale Antiphlogistika (NSAID), wie auf Acetylsalizylsäure, werden in Kombination mit Polyposis nasi und Asthma bronchiale als Morbus Widal (Samter Trias, Morbus Samter) bezeichnet, wobei der Begriff Aspirin-exacerbated Respiratory Disease (AERD) neuerdings favorisiert wird. Diese Pseudoallergie tritt bei bis zu 10% aller Asthmatiker auf und verursacht schwerwiegende, lebensbedrohliche oder anaphylaktische Episoden. Es handelt sich hierbei nicht um einen IgE-vermittelten Mechanismus, sondern um eine erworbene Dysbalance im Arachidonsäurestoffwechsel, welche durch die Aufnahme von nichtsteroidalen Antiphlogistika akut verstärkt wird. Die Patienten leiden auch ohne Einnahme von NSAID neben der genannten Symptomtrias an nasaler Obstruktion, wässriger Rhinorrhoe, Hyposmie, Urtikaria und/oder Angioödemen. Die Diagnose einer Analgetikaintoleranz lässt sich nur mit Hilfe eines Provokationstests stellen. Die Grundkrankheit wird mit topischen und systemischen Glukokortikosteroiden, β2-Sympathomimetika und Antileukotrienen behandelt, NSAID sind streng zu meiden. Eine spezifische Therapie steht mit der adaptiven Acetylsalizylsäuredesaktivierung zur Verfügung, von der gerade Patienten mit ansonsten behandlungsresistenten Verläufen profitieren.
Abstract
The full clinical picture of aspirin intolerance – the association of aspirin-induced bronchial asthma, aspirin sensitivity and nasal polyps – has been described as Morbus Widal or later as the “Samter triad”. Today the term Aspirin-exacerbated respiratory disease (AERD) is preferred to account for the progressive nature of this inflammatory airway condition with its unrelenting course even in the absence of non steroidal anti-inflammatory drugs (NSAID). This acquired idiosyncrasy appears to be related to an abnormal arachidonic acid metabolism. Epidemiological data suggests that 10% of all asthmatics do react with life-threatening asthma-attacks after the ingestion of aspirin (ASA) or other NSAID. Some asthmatics with nasal polyposis have been reported to suffer from aspirin intolerance. Although the exact mechanism is still unclear, it is unlikely that the pathogenesis is IgE-mediated. Patients often report chronic nasal obstruction, hyposmia, chronic rhinorrhoea, orbital edema and urticaria with flushing after the ingestion of NSAID. While a typical history and endoscopic findings can be suggestive of AERD, a definite diagnosis relies on appropriate challenge tests. AERD is often refractory to standard asthma treatment with systemic and inhaled steroids, β2-agonists, leukotrien-antagonists. Adaptive desactivation can induce a reversible tolerance to NSAID which also leads to an improvement in signs and symptoms of the underlying AERD.
Literatur
Arm JP, Austen KF (2002) Leukotriene receptors and aspirin sensitivity. N Engl J Med 347:1524–1526
Babu KS, Salvi SS (2000) Aspirin and asthma. Chest 118:1470–1476
Berges-Gimeno MP, Simon RA, Stevenson DD (2002) The natural history and clinical characteristics of aspirin-exacerbated respiratory disease. Ann Allergy Asthma Immunol 89:474–478
Berges-Gimeno MP, Simon RA, Stevenson DD (2003) Long-term treatment with aspirin desensitization in asthmatic patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol 111:180–186
Cowburn AS, Sladek K, Soja J et al (1998) Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma. J Clin Invest 101:834–846
Dahlen SE (2006) Treatment of asthma with antileukotrienes: first line or last resort therapy? Eur J Pharmacol 533:40–56
Dollner R, Klimek L, Pfaar O et al (2007) In-vitro-Testverfahren bei Analgetika-Intoleranz. Allergologie 30:240–248
Gosepath J, Schaefer D, Amedee RG, Mann WJ (2001) Individual monitoring of aspirin desensitization. Arch Otolaryngol Head Neck Surg 127:316–321
Klimek L, Pfaar O (2009) Aspirin intolerance: does desensitization alter the course of the disease? Immunol Allergy Clin North Am 29:669–675
Lee JY, Simon RA, Stevenson DD (2007) Selection of aspirin dosages for aspirin desensitization treatment in patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol 119:157–164
Makowska JS, Grzegorczyk J, Bienkiewicz B et al (2008) Systemic responses after bronchial aspirin challenge in sensitive patients with asthma. J Allergy Clin Immunol 121:348–354
May A, Weber A, Gall H et al (1999) Means of increasing sensitivity of an in vitro diagnostic test for aspirin intolerance. Clin Exp Allergy 29:1402–1411
Molnar-Gabor E, Endreffy E, Rozsasi A (2000) HLA-DRB1, -DQA1, and -DQB1 genotypes in patients with nasal polyposis. Laryngoscope 110:422–425
Nizankowska-Mogilnicka E, Bochenek G, Mastalerz L et al (2007) EAACI/GA2LEN guideline: aspirin provocation tests for diagnosis of aspirin hypersensitivity. Allergy 62:1111–1118
Parikh AA, Scadding GK (2005) Intranasal lysine-aspirin in aspirin-sensitive nasal polyposis: a controlled trial. Laryngoscope 115:1385–1390
Pfaar O, Klimek L (2006) Aspirin desensitization in aspirin intolerance: update on current standards and recent improvements. Curr Opin Allergy Clin Immunol 6:161–166
Pfaar O, Klimek L (2006) Eicosanoids, aspirin-intolerance and the upper airways–current standards and recent improvements of the desensitization therapy. J Physiol Pharmacol 57 (Suppl 12):5–13
Picado C (2002) Aspirin intolerance and nasal polyposis. Curr Allergy Asthma Rep 2:488–493
Rozsasi A, Polzehl D, Deutschle T et al (2008) Long-term treatment with aspirin desensitization: a prospective clinical trial comparing 100 and 300 mg aspirin daily. Allergy 63:1228–1234
Samter M, Beers RF Jr (1968) Intolerance to aspirin. Clinical studies and consideration of its pathogenesis. Ann Intern Med 68:975–983
Schafer D, Lindenthal U, Wagner M et al (1996) Effect of prostaglandin E2 on eicosanoid release by human bronchial biopsy specimens from normal and inflamed mucosa. Thorax 51:919–923
Stevenson DD (2009) Aspirin sensitivity and desensitization for asthma and sinusitis. Curr Allergy Asthma Rep 9:155–163
Stevenson DD, Hankammer MA, Mathison DA et al (1996) Aspirin desensitization treatment of aspirin-sensitive patients with rhinosinusitis-asthma: long-term outcomes. J Allergy Clin Immunol 98:751–758
Szczeklik A, Nizankowska E, Bochenek G et al (2001) Safety of a specific COX-2 inhibitor in aspirin-induced asthma. Clin Exp Allergy 31:219–225
Szczeklik A, Nizankowska E, Duplaga M (2000) Natural history of aspirin-induced asthma. AIANE Investigators. European network on aspirin-induced asthma. Eur Respir J 16:432–436
Szczeklik A, Sanak M, Nizankowska-Mogilnicka E, Kielbasa B (2004) Aspirin intolerance and the cyclooxygenase-leukotriene pathways. Curr Opin Pulm Med 10:51–56
Szczeklik A, Stevenson DD (1999) Aspirin-induced asthma: advances in pathogenesis and management. J Allergy Clin Immunol 104:5–13
Weck AL de, Sanz ML (2004) Cellular Allergen Stimulation Test (CAST) 2003, a review. J Investig Allergol Clin Immunol 14:253–273
Widal F, Abrami P, Lermoyez J (1987) First complete description of the aspirin idiosyncrasy-asthma-nasal polyposis syndrome (plus urticaria) 1922 (with a note on aspirin desensitization). J Asthma 24:297–300
Zeiss C, Lockey RF (1976) Refractory period to aspirin in a patient with aspirin-induced asthma. J Allergy Clin Immunol 57:440–448
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Umbreit, C., Virchow, J., Thorn, C. et al. Analgetikaintoleranz. Internist 51, 1196–1201 (2010). https://doi.org/10.1007/s00108-010-2661-y
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DOI: https://doi.org/10.1007/s00108-010-2661-y