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

Abstract 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.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title annals of allergy, asthma & immunology : official publication of the american college of allergy, asthma, & immunology
Publication Year Start




PMID- 28668243
OWN - NLM
STAT- In-Process
DA  - 20170702
LR  - 20170702
IS  - 1534-4436 (Electronic)
IS  - 1081-1206 (Linking)
VI  - 119
IP  - 1
DP  - 2017 Jul
TI  - Effect of misoprostol on patients with aspirin-exacerbated respiratory disease
      undergoing aspirin challenge and desensitization.
PG  - 71-76
LID - S1081-1206(17)30357-5 [pii]
LID - 10.1016/j.anai.2017.05.003 [doi]
AB  - 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 mug) 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.
CI  - Copyright (c) 2017 American College of Allergy, Asthma & Immunology. Published by
      Elsevier Inc. All rights reserved.
FAU - Walters, Kristen M
AU  - Walters KM
AD  - Scripps Clinic, San Diego, California. Electronic address: [email protected]
FAU - Simon, Ronald A
AU  - Simon RA
AD  - Scripps Clinic, San Diego, California.
FAU - Woessner, Katharine M
AU  - Woessner KM
AD  - Scripps Clinic, San Diego, California.
FAU - Wineinger, Nathan E
AU  - Wineinger NE
AD  - Scripps Translational Science Institute, La Jolla, California.
FAU - White, Andrew A
AU  - White AA
AD  - Scripps Clinic, San Diego, California.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Ann Allergy Asthma Immunol
JT  - Annals of allergy, asthma & immunology : official publication of the American
      College of Allergy, Asthma, & Immunology
JID - 9503580
EDAT- 2017/07/03 06:00
MHDA- 2017/07/03 06:00
CRDT- 2017/07/03 06:00
PHST- 2017/03/01 [received]
PHST- 2017/04/21 [revised]
PHST- 2017/05/01 [accepted]
AID - S1081-1206(17)30357-5 [pii]
AID - 10.1016/j.anai.2017.05.003 [doi]
PST - ppublish
SO  - Ann Allergy Asthma Immunol. 2017 Jul;119(1):71-76. doi:
      10.1016/j.anai.2017.05.003.