Medline ® Abstract for Reference 39
of 'Laboratory tests to support the clinical diagnosis of anaphylaxis'
Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA-sensitive patients.
Kowalski ML, Grzegorczyk J, Wojciechowska B, Poniatowska M
Clin Exp Allergy. 1996;26(7):807.
BACKGROUND: Although the mechanism of aspirin-sensitivity seems to be related to inhibition of cyclo-oxygenase by aspirin (ASA), the chain of biochemical events leading to the ASA-induced adverse reaction is not clear, and the contribution of particular mediators and inflammatory cells has not been elucidated.
OBJECTIVES: To investigate the involvement of secretory, vascular and cellular mechanisms in the pathophysiology of nasal reactions to aspirin.
METHODS: Six patients with ASA-sensitive asthma/rhinosinusitis and seven ASA-tolerant patients were challenged intranasaly with saline and lysine-acetylsalicylic acid (Lys-ASA) 12 mg, on separate occasions. Nasal lavages were obtained before, and then every 15 min after challenges, and analysed for biochemical and cellular composition.
RESULTS: Lys-ASA challenge caused rhinorrhoea, sneezing and nasal congestion with parallel increases in total protein and albumin concentration, albumin % and lysozyme activity in the nasal secretions of ASA-sensitive patients. Concomitant with clinical symptoms, an influx of leucocytes into nasal secretions occurred with significant enrichment in eosinophils (mean prechallenge: 24 +/- 12%, postsaline 27 +/- 9%, postLys-ASA 51 +/- 10%; P<0.03). The influx of eosinophils into nasal secretions was associated with a remarkable increase in Eosinophil Cationic Protein (ECP) immunoreactivity in five of six patients (mean 9.3 +/- 3.8 micrograms/L and 140.9 +/- 45.8 micrograms/mL before and after Lys-ASA, respectively). At the peak of ASA-induced symptoms an increase in the tryptase level was also observed in five of six patients (mean pre-challenge: 2 +/- 0.1 U/L; postLys-ASA 16 +/- 5 U/L; P<0.01) suggesting activation of mucosal mast cells. In ASA-tolerant patients Lys-ASA did not induce significant symptoms or changes in the biochemical and cellular composition of nasal secretions.
CONCLUSION: The results show that the ASA-induced nasal adverse reaction involves changes in vascular permeability and serous cell secretion. Both activated eosinophils and mast cells may contribute to the pathophysiology of the ASA-induced reaction in the nasal mucosa.
Department of Clinical Immunology and Allergy, Faculty of Medicine, Medical University of Lódz, Poland.