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

• Published in: Journal of allergy and clinical immunology Vol. 134; no. 4; pp. 883 - 890
• Main Authors: Świerczyńska-Krępa, Monika, MD, PhD, Sanak, Marek, MD, PhD, Bochenek, Grażyna, MD, PhD, Stręk, Paweł, MD, PhD, Ćmiel, Adam, PhD, Gielicz, Anna, PhD, Plutecka, Hanna, PhD, Szczeklik, Andrzej, MD, PhD, Niżankowska-Mogilnicka, Ewa, MD, PhD
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.10.2014; Elsevier; Elsevier Limited
• Subjects: Administration, Oral; Adult; Aged; Allergens - immunology; Allergy and Immunology; Aspirin; Aspirin - administration & dosage; Aspirin - immunology; Aspirin-induced asthma; aspirin-tolerant asthma; Asthma; Asthma - diagnosis; Asthma - immunology; Asthma - therapy; Asthma, Aspirin-Induced - diagnosis; Asthma, Aspirin-Induced - immunology; Asthma, Aspirin-Induced - therapy; Biological and medical sciences; Chronic Disease; Chronic obstructive pulmonary disease, asthma; Desensitization, Immunologic - methods; Dinoprost - blood; Double-Blind Method; Drug dosages; Drug therapy; Eosinophils - immunology; Female; Follow-Up Studies; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunopathology; Leukotriene E4 - urine; Male; Medical sciences; Middle Aged; Nasal Polyps - diagnosis; Nasal Polyps - immunology; Nasal Polyps - therapy; oral aspirin desensitization; Pilot Projects; Pneumology; Prostaglandin D2 - blood; Rhinitis - diagnosis; Rhinitis - immunology; Rhinitis - therapy; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Sinusitis - diagnosis; Sinusitis - immunology; Sinusitis - therapy; Spirometry; Treatment Outcome; uLTE 4; 9α,11β-PGF 2; Cysteinyl leukotriene; NSAID; LTE 4; Urinary LTE 4; L-ASA; Acetylsalicylic acid; ASA; Aspirin-induced asthma; Computed tomography; Aspirin desensitization; AIA; 9α,11β-Prostaglandin F 2; Leukotriene E 4; Lysine-aspirin; AD; Prostaglandin; Inhaled corticosteroid; SNOT20; ATA; cysLT; ACQ; Asthma Control Questionnaire; PEF; CT; Peak nasal inspiratory flow; oral aspirin desensitization; Nonsteroidal anti-inflammatory drug; PG; aspirin-tolerant asthma; ICS; Peak expiratory flow; Sino-Nasal Outcome Test; PNIF; 9α,11β-PGF2; LTE4; uLTE4; Human; Lung disease; Prostaglandin-endoperoxide synthase; Immunopathology; Desensitization; Enzyme; Respiratory disease; Oral administration; Enzyme inhibitor; Antiplatelet agent; Asthma; Immunology; Double blind study; Bronchus disease; Obstructive pulmonary disease; Oxidoreductases; Salicylates
• ISSN: 0091-6749; 1097-6825
• DOI: 10.1016/j.jaci.2014.02.041

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 anti-inflammatory 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, placebo-controlled 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 9α,11β-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 9α,11β-PGF2 levels after AD. Conclusion The clinically beneficial effects of AD on nasal and bronchial symptoms occurred only in the patients with AIA.