alexa Hypothetical Mechanism of Aspirin-Exacerbated Respirato
ISSN: 2155-6121

Journal of Allergy & Therapy
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Review Article

Hypothetical Mechanism of Aspirin-Exacerbated Respiratory Disease Based on Recent Investigations of Gene Polymorphisms in Japanese Patients

Motohiro Kurosawa1,2*, Yujin Sutoh3, Tatsuo Yukawa4, Soichiro Hozawa5 and Eijin Sutoh1

1Department of Allergy and Respiratory Medicine, Sutoh Hospital, Annaka-shi, Gunma, Japan

2Gunma Institute for Allergy and Asthma, Gunma, Japan

3Department of Surgery, National Hospital Organization Takasaki General Medical Center, Takasaki, Gunma, Japan

4Yukawa Clinic of Internal Medicine, Tochigi, Japan

5Hiroshima Allergy and Respiratory Clinic, Hiroshima, Japan

*Corresponding Author:
Kurosawa M
Department of Allergy and Respiratory Medicine, Sutoh Hospital
3532-5 Annaka, Annaka-shi, Gunma 379-0116, Japan
Tel: +81-27-382-3131
Fax: +81-27-382-6568
E-mail: [email protected]

Received date: December 05, 2015; Accepted date: February 03, 2016; Published date: February 10, 2016

Citation: Kurosawa M, Sutoh Y, Yukawa T, Hozawa S, Sutoh E (2016) Hypothetical Mechanism of Aspirin-Exacerbated Respiratory Disease Based on Recent Investigations of Gene Polymorphisms in Japanese Patients. J Allergy Ther 7:230. doi:10.4172/2155-6121.1000230

Copyright: © 2016 Kurosawa M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



Aspirin-exacerbated respiratory disease (AERD) is characterized by severe asthmatic attack after taking aspirin and/or nonsteroidal anti-inflammatory drugs (NSAIDs). The typical patient with AERD is an adult who develops refractory chronic rhinitis in the third or fourth decade of life. Natural history and clinical features of AERD indicates that during the evaluation of chronic rhinitis persistent bronchial asthma develops, and finally after exposure to NSAID acute respiratory reactions begin to occur. The inhibitory action of aspirin and/or NSAIDs on cyclooxygenase activity may cause diversion to the 5-lipoxygenase pathway, which leads to the overproduction of cysteinyl leukotrienes (LTs). Thus, a general consensus exists that increased levels of cysteinyl LTs are key inflammatory mediators in AERD. As aspirin intolerance is found in a specific population, genetic predisposition has been considered as a crucial determinant. Investigations on candidate genes have been concentrated especially on cysteinyl LTs-related genes, however conflicting results have been reported. So, future areas of investigations need to focus on comprehensive approaches towards other genetic biomarkers. We’ve recently reported possible presence of other gene polymorphisms in Japanese patients with AERD. The natural history and clinical characteristics of AERD indicate that the respiratory mucosal inflammatory process in AERD begins and continues in the absence of ongoing or even intermittent exposure to NSAIDs. So, in this review, we propose a hypothetical progress of AERD over time based on mainly the results of our investigations, and present a schematically sketching the course of NSAIDs-triggered hypersensitivity with genes, such as asthma-associated genes, that may initiate susceptibility to AERD, and that may accelerate pathogenesis and induce onset of AERD. The findings of our studies were based on small-sized samples from a Japanese population, and future validation studies in independent populations are required to provide reassurance about our hypothesis.


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