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Clinical & Experimental Allergy

Urinary concentrations of 15-epimer of lipoxin A4 are lower in patients with aspirin-intolerant compared with aspirin-tolerant asthma

Authors

  • H. Yamaguchi,

    1. Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
    2. Division of Respiratory and Infectious Diseases, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
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  • N. Higashi,

    1. Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
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  • H. Mita,

    1. Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
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  • E. Ono,

    1. Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
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  • Y. Komase,

    1. Division of Respiratory and Infectious Diseases, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
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  • T. Nakagawa,

    1. Kawazoe Clinic, Shirahama, Wakayama, Japan
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  • T. Miyazawa,

    1. Division of Respiratory and Infectious Diseases, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
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  • K. Akiyama,

    1. Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
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  • M. Taniguchi

    Corresponding author
    • Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan
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  • We hereby declare no financial relationship with any technological and/or pharmaceutical manufacturer that has interest in the subject matter or materials discussed in this manuscript.

Correspondence:

Masami Taniguchi

Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital

18-1 Sakuradai, Sagamihara, Kanagawa 252-0392, Japan

E-mail: m-taniguchi@sagamihara-hosp.gr.jp

Summary

Background

Although an abnormality in arachidonic acid metabolism may be responsible for aspirin-intolerant asthma (AIA), there is little knowledge about the concentrations of urinary lipoxin A4 (LXA4) and the 15-epimer of LXA4 (15-epi-LXA4) in relation to asthma severity in AIA subjects.

Objective

The purpose of this study is to estimate urinary LXA4 and the 15-epimer concentrations to investigate lipoxins in AIA.

Methods

In this study, we examined AIA, aspirin-tolerant asthma (ATA) and healthy control groups. The AIA and ATA groups were subdivided into the severe asthma and non-severe asthma subgroups. Urinary LXA4, 15-epi-LXA4 and leukotriene E4 (LTE4) were quantified using enzyme immunoassay after separating these compounds using high-performance liquid chromatography.

Results

The urinary LXA4 concentration was significantly lower than the 15-epi-LXA4 concentration in the asthmatic subjects. The AIA group showed significantly lower urinary 15-epi-LXA4 (< 0.01) and higher urinary LTE4 concentrations (< 0.05) than the ATA group. Comparison of 15-epi-LXA4 concentrations between the severe asthmatic and non-severe asthmatic subjects in the AIA and ATA groups revealed that the decreased 15-epi-LXA4 concentration may be related to aspirin intolerance, but not asthma severity. Receiver operator characteristic curves demonstrated that the concentration ratio of LTE4 to 15-epi-LXA4 was superior to 15-epi-LXA4 concentration and LTE4 concentration as a predictive factor for aspirin intolerance.

Conclusions and Clinical Relevance

We have demonstrated for the first time that urinary 15-epi-LXA4 concentration is significantly higher than LXA4 concentration in both the AIA and ATA groups. 15-Epi-LXA4 concentration was significantly lower in the AIA group with an increased urinary LTE4 concentration than in the ATA group. An imbalance between proinflammatory cysteinyl-leukotrienes and anti-inflammatory 15-epi-LXA4 may be involved in AIA pathogenesis.

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