Allergology International
Online ISSN : 1440-1592
Print ISSN : 1323-8930
ISSN-L : 1323-8930
REVIEW ARTICLE
Aspirin-Intolerant Asthma (AIA) Assessment Using the Urinary Biomarkers, Leukotriene E4 (LTE4) and Prostaglandin D2 (PGD2) Metabolites
Noritaka HigashiMasami TaniguchiHaruhisa MitaHiromichi YamaguchiEmiko OnoKazuo Akiyama
Author information
JOURNALS FREE ACCESS

2012 Volume 61 Issue 3 Pages 393-403

Details
Abstract

The clinical syndrome of aspirin-intolerant asthma (AIA) is characterized by aspirin/nonsteroidal anti-inflammatory drug intolerance, bronchial asthma, and chronic rhinosinusitis with nasal polyposis. AIA reactions are evidently triggered by pharmacological effect of cyclooxygenase-1 inhibitors. Urine sampling is a non-invasive research tool for time-course measurements in clinical investigations. The urinary stable metabolite concentration of arachidonic acid products provides a time-integrated estimate of the production of the parent compounds in vivo. AIA patients exhibits significantly higher urinary concentrations of leukotriene E4 (LTE4) and 1,15-dioxo-9α-hydroxy-2,3,4,5-tetranorprostan-1,20-dioic acid (tetranor-PGDM), a newly identified metabolite of PGD2, at baseline. This finding suggests the possibility that increased mast cell activation is involved in the pathophysiology of AIA even in a clinically stable condition. In addition, lower urinary concentrations of primary prostaglandin E2 and 15-epimer of lipoxin A4 at baseline in the AIA patients suggest that the impaired anti-inflammatory elements may also contribute to the severe clinical outcome of AIA. During the AIA reaction, the urinary concentrations of LTE4 and PGD2 metabolites, including tetranor-PGDM significantly and correlatively increase. It is considered that mast cell activation probably is a pathophysiologic hallmark of AIA. However, despite the fact that cyclooxygenease-1 is the dominant in vivo PGD2 biosynthetic pathway, the precise mechanism underlying the PGD2 overproduction resulting from the pharmacological effect of cyclooxygenease-1 inhibitors in AIA remains unknown. A comprehensive analysis of the urinary concentration of inflammatory mediators may afford a new research target in elucidating the pathophysiology of AIA.

Information related to the author

This article cannot obtain the latest cited-by information.

© 2012 by Japanese Society of Allergology
Previous article Next article
feedback
Top