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  • 1
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: A state of tolerance to aspirin (ASA) was induced in 10 aspirin-sensitive patients by daily administration of incremental doses of ASA. No adverse reactions were reported. The initial dose (from 5 to 60 mg) was gradually increased each day up to 300 mg and then doubled. 50 mg indomethacin given the day after administration of 600 mg ASA did not elicit any symptom of intolerance. The authors discuss a possible mechanism of tolerance to aspirin in ASA-sensitive asthmatics after ASA administration, suggesting that it might be connected either with inhibition of the lipooxygenetic pathway of arachidonic acid metabolism or with blockade of the cyclooxygenase supplementary binding site by salicylic acid, a product of acetylsalicylic acid hydrolysis. This would prevent aspirin from binding with the catalytic cyclooxygenase site.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In a group of aspirin-sensitive asthmatics we studied skin weal and flare responses to intradermal injections of compound 48/80 and histamine during oral aspirin (ASA) provocation and after ASA “desensitisation”. During provocation (bronchospasm accompanied by naso-ocular symptoms) the mean weal area after compound 48/80 increased to about 42.4% (P 〈 0.05). Neither the threshold (provocative) doses of ASA nor 600 mg ASA, when given after ASA-desensitisation, significantly influenced the weal reactions to compound 48/80 (mean changes of area were –1.8% and –16.5% respectively). Aspirin did not change flare reactions to compound 48/80 and weal and flare reactions to histamine on any of the three study occasions. Initial (pre-aspirin) weal reactions to compound 48/80 after desensitisation to the threshold ASA doses were significantly reduced, but after desensitisation to 600 mg ASA were significantly increased as compared with the reactions before. These data suggest that ASA-“desensitisation” may influence the skin reactivity to non-specific mast cell degranulating stimulus in ASA-sensitive asthmatics.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 11 (1981), S. 74-75 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bronchial challenge with polymyxin B caused a significant bronchoconstriction in 85% of atopic asthmatics. In all atopic asthmatics in whom inhalation of polymyxin B elicited bronchoconstriction, a significant, although not always parallel to the grade of bronchoconstriction, increase in histaminemia was observed. If bronchoconstriction was not elicited, the increase in histaminemia did not occur. It constitutes evidence that the bronchoconstricting effect of polymyxin B is exclusively due to degranulation of mast cells and that histamine released in the bronchi can increase the concentration of histamine in the blood.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To determine the role of mast cells in aspirin-induced bronchoconstriction, venous histaminemia was measured in 17 aspirin-sensitive patients before and after administration of aspirin. Ventilatory disturbances were measured spirographically. Venous histaminemia was determined according to Lorenz. In 11 patients the mean increase of histaminemia was from 39.6 ng/ml to 107.0 ng/ml. In the remaining 6 patients no change in histaminemia was observed after the challenge. In patients exhibiting the increase of histaminemia, symptoms of hypersensitivity to aspirin, other than dyspnea, were more common and stronger. The authors discuss a possible relationship of the aspirin effect, disturbances in prostaglandin synthesis and histamine release.
    Type of Medium: Electronic Resource
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