Literature DB >> 9494450

Cromolyn sodium prevents bronchoconstriction and urinary LTE4 excretion in aspirin-induced asthma.

S Yoshida1, H Amayasu, H Sakamoto, K Onuma, T Shoji, H Nakagawa, T Tajima.   

Abstract

BACKGROUND: Inhalation of cromolyn sodium protects against sulpyrine-induced bronchoconstriction and prevents urinary leukotriene E4 (u-LTE4) excretion in aspirin-induced asthma.
OBJECTIVE: This study was designed to investigate the protective effect of cromolyn sodium on airway responsiveness to the sulpyrine provocation test, and to investigate whether this protective activity is associated with a reduction in aspirin-induced urinary excretion of LTE4, a marker of the cysteinyl leukotriene overproduction that participates in the pathogenesis of aspirin-induced asthma.
METHODS: We evaluated the effects of pretreatment with cromolyn sodium on bronchoconstriction precipitated by inhalation of sulpyrine in ten adult patients with mild aspirin-induced asthma. Those who were in stable clinical condition and were hyperresponsive to sulpyrine provocation test were allocated to this study. Urinary leukotriene E4 was measured using combined reverse phase high performance liquid chromatography (rp-HPLC)/enzyme immunoassay.
RESULTS: Inhaled cromolyn sodium protects against aspirin-induced attacks of asthma through mechanisms not related to the bronchodilator property, but related to the improvement of the bronchial hypersensitivity, almost completely in all patients (P < .001). By contrast, after cromolyn sodium the maximum level of u-LTE4 was significantly lower than control (P < .05).
CONCLUSION: Our results suggest for the first time that inhaled cromolyn sodium is one of the most useful inhibitors of aspirin-induced bronchoconstriction, probably acting by inhibiting the release of cysteinyl leukotrienes, and possibly other chemical mediators, by bronchial inflammatory cells.

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Year:  1998        PMID: 9494450     DOI: 10.1016/S1081-1206(10)62951-1

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


  10 in total

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3.  Prostaglandin D₂: a dominant mediator of aspirin-exacerbated respiratory disease.

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Review 4.  Aspirin sensitivity: Lessons in the regulation (and dysregulation) of mast cell function.

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6.  Prostaglandin E2 deficiency causes a phenotype of aspirin sensitivity that depends on platelets and cysteinyl leukotrienes.

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7.  Aspirin-Exacerbated Respiratory Disease Involves a Cysteinyl Leukotriene-Driven IL-33-Mediated Mast Cell Activation Pathway.

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8.  A trial of type 12 purinergic (P2Y12) receptor inhibition with prasugrel identifies a potentially distinct endotype of patients with aspirin-exacerbated respiratory disease.

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Review 9.  Cysteinyl leukotrienes and their receptors; emerging concepts.

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Journal:  Allergy Asthma Immunol Res       Date:  2014-05-27       Impact factor: 5.764

10.  The whole-genome expression analysis of peripheral blood mononuclear cells from aspirin sensitive asthmatics versus aspirin tolerant patients and healthy donors after in vitro aspirin challenge.

Authors:  Joanna Wieczfinska; Dorota Kacprzak; Karolina Pospiech; Milena Sokolowska; Magdalena Nowakowska; Ewa Pniewska; Andrzej Bednarek; Izabela Kuprys-Lipinska; Piotr Kuna; Rafal Pawliczak
Journal:  Respir Res       Date:  2015-12-09
  10 in total

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