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Tytuł pozycji:

Aspirin desensitization in patients with aspirin-induced and aspirin-tolerant asthma : a double-blind study

Tytuł:
Aspirin desensitization in patients with aspirin-induced and aspirin-tolerant asthma : a double-blind study
Autorzy:
Cmiel, Adam
Plutecka, Hanna
Sanak, Marek
Świerczyńska, Monika
Szczeklik, Andrzej
Bochenek, Grażyna
Gielicz, Anna
Stręk, Paweł
Niżankowska-Mogilnicka, Ewa
Data publikacji:
2014
Słowa kluczowe:
aspirin-induced asthma
aspirin-tolerant asthma
oral aspirin desensitization
Język:
angielski
ISBN, ISSN:
00916749
Prawa:
Udzielam licencji. Uznanie autorstwa - Użycie niekomercyjne - Bez utworów zależnych 4.0 Międzynarodowa
http://creativecommons.org/licenses/by-nc-nd/4.0/legalcode.pl
Dostawca treści:
Repozytorium Uniwersytetu Jagiellońskiego
Artykuł
Background: Numerous open trials have demonstrated the beneficial clinical effects of aspirin desensitization (AD) in patients with aspirin-induced asthma (AIA). These beneficial effects might be attributable to aspirin’s potent antiinflammatory properties, but that supposition requires further corroboration. Objective: We sought to compare the clinical and biochemical responses to chronic oral AD in 20 patients with AIA and 14 patients with aspirin-tolerant asthma (ATA). All of the patients had chronic rhinosinusitis and nasal polyposis, and these responses were investigated in a pilot, double-blind, placebocontrolled study. Methods: Twelve patients with AIA and 6 patients with ATA were randomly assigned to receive 624 mg of aspirin, and 8 patients with AIA and 8 patients with ATA received placebo. Both aspirin and placebo were administered once daily for 6 months. Nasal symptoms, Sino-Nasal Outcome Test (SNOT20) scores, peak nasal inspiratory flows, Asthma Control Questionnaire scores, spirometric parameters, peak expiratory flows, blood eosinophilia, and corticosteroid doses were assessed on a monthly basis. Levels of urinary leukotriene E4 and the stable plasma prostaglandin (PG) D2 metabolite 9a,11b-PGF2 were evaluated at baseline and after 1, 3, 5, and 6 months. Results: Only the patients with AIA subjected to AD reported improvements in smell and reductions in sneezing and nasal blockade. The SNOT20 and Asthma Control Questionnaire scores of these patients decreased, and their peak nasal inspiratory flows increased. The dosages of inhaled corticosteroids were reduced. There were no changes in leukotriene E4 or 9a,11b-PGF2 levels after AD. Conclusion: The clinically beneficial effects of AD on nasal and bronchial symptoms occurred only in the patients with AIA.

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