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Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA‐sensitive patients
Author(s) -
KOWALSKI M. L.,
GRZEGORCZYK J.,
WOJCIECHOWSKA B.,
PONIATOWSKA M.
Publication year - 1996
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1996.tb00612.x
Subject(s) - medicine , aspirin , eosinophil , tryptase , nasal provocation test , eosinophil cationic protein , nasal administration , nasal lavage , allergy , pathophysiology , albumin , nasal cavity , immunology , mucous membrane of nose , pharmacology , saline , mast cell , asthma , surgery , allergen
Summary 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) 12mg, on separate occasions. Nasal lavages were obtained before, and then every 15min 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%, postsatine 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 μg/L and 140.9 ± 45.8 μg/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 prechallenge: 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.