Literature DB >> 28668243

Effect of misoprostol on patients with aspirin-exacerbated respiratory disease undergoing aspirin challenge and desensitization.

Kristen M Walters1, Ronald A Simon2, Katharine M Woessner2, Nathan E Wineinger3, Andrew A White2.   

Abstract

BACKGROUND: Prostaglandin E2 (PGE2) is an anti-inflammatory compound that inhibits 5-lipoxygenase activity. Diminished PGE2 regulation in aspirin-exacerbated respiratory disease (AERD) leads to respiratory reactions on cyclooxygenase 1 inhibition. In vitro studies have found that exogenous PGE2 stabilizes inflammatory mediator release.
OBJECTIVE: To examine whether misoprostol (oral prostaglandin E1 analogue) use during aspirin challenge and desensitization might decrease the severity of aspirin-induced symptoms and make desensitization safer for patients with AERD.
METHODS: Forty-five patients undergoing aspirin challenge and/or desensitization were randomized to misoprostol (n = 30) or placebo (n = 15) and compared with a group of historical controls (n = 31). Misoprostol (200 μg) was administered at 30 minutes, 90 minutes, and 4 hours after the first dose of nasal ketorolac. Measured end points included change in forced expiratory volume in 1 second (FEV1), peak nasal inspiratory flow rate (PNIF), number of treatments received for induced reactions, and adverse gastrointestinal effects.
RESULTS: A difference in FEV1 and PNIF reduction was detected between misoprostol and placebo (P = .03) and misoprostol and historical controls (P = .01), respectively, during nasal ketorolac challenge. No difference was detected among aspirin reactors. Among all reactors, no difference in magnitude was found for FEV1 (P = .13) or PNIF (P = .07) reduction across all 3 groups. Total treatment requirement was similar (P = .14). Patients receiving misoprostol were more likely to report adverse gastrointestinal effects (P = .02).
CONCLUSION: The addition of misoprostol to current aspirin challenge and/or desensitization protocols reveals no protective effect in reducing the intensity of nonsteroidal anti-inflammatory drug-induced symptoms and is not recommended based on the findings in this study.
Copyright © 2017 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.

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Year:  2017        PMID: 28668243     DOI: 10.1016/j.anai.2017.05.003

Source DB:  PubMed          Journal:  Ann Allergy Asthma Immunol        ISSN: 1081-1206            Impact factor:   6.347


  4 in total

Review 1.  Prostaglandins in asthma and allergic diseases.

Authors:  R Stokes Peebles
Journal:  Pharmacol Ther       Date:  2018-08-03       Impact factor: 12.310

Review 2.  The role of aspirin desensitization followed by oral aspirin therapy in managing patients with aspirin-exacerbated respiratory disease: A Work Group Report from the Rhinitis, Rhinosinusitis and Ocular Allergy Committee of the American Academy of Allergy, Asthma & Immunology.

Authors:  Whitney W Stevens; Elina Jerschow; Alan P Baptist; Larry Borish; John V Bosso; Kathleen M Buchheit; Katherine N Cahill; Paloma Campo; Seong H Cho; Anjeni Keswani; Joshua M Levy; Anil Nanda; Tanya M Laidlaw; Andrew A White
Journal:  J Allergy Clin Immunol       Date:  2020-12-09       Impact factor: 10.793

3.  Misoprostol complications in second-trimester termination of pregnancy among women with a history of more than one cesarean section.

Authors:  Marzieh Jamali; Mahmood Bakhtiyari; Fatemeh Arab; Masoumeh Mirzamoradi
Journal:  Obstet Gynecol Sci       Date:  2020-04-21

Review 4.  The Biology of Prostaglandins and Their Role as a Target for Allergic Airway Disease Therapy.

Authors:  Kijeong Lee; Sang Hag Lee; Tae Hoon Kim
Journal:  Int J Mol Sci       Date:  2020-03-08       Impact factor: 5.923

  4 in total

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