Literature DB >> 12704352

A controlled study of 9alpha,11beta-PGF2 (a prostaglandin D2 metabolite) in plasma and urine of patients with bronchial asthma and healthy controls after aspirin challenge.

Grazyna Bochenek1, Krzysztof Nagraba, Ewa Nizankowska, Andrzej Szczeklik.   

Abstract

BACKGROUND: Prostaglandin D(2) (PGD(2)) is the predominant cyclooxygenase product of mast cells, the number of which is increased in bronchial asthma. Release of PGD(2) might reflect mast cell activation and disordered function of the asthmatic lung.
OBJECTIVE: We sought to determine blood and urinary levels of 9alpha,11beta-PGF(2), a major stable PGD(2) metabolite in 2 well-defined phenotypes of asthma, aspirin-induced asthma (AIA) and aspirin-tolerant asthma (ATA), and in healthy control subjects and to study the effects of aspirin on PGD(2) release.
METHODS: Using gas chromatography/mass spectrometry, we determined plasma and urinary concentrations of 9alpha,11beta-PGF(2) at baseline in 131 stable asthmatic patients, 65 of whom had AIA and 66 of whom had ATA. Fifty healthy nonatopic subjects served as the control group. The measurements were also performed after an aspirin challenge in 26 of 65 patients with AIA and in 24 of 50 control subjects.
RESULTS: At baseline, patients with AIA had significantly higher plasma levels of 9alpha,11beta-PGF(2) than either patients with ATA or healthy subjects. A similar significant elevation of serum tryptase was observed in patients with AIA compared with patients with ATA and control subjects. Mean urinary 9alpha,11beta-PGF(2) values did not differ among the 3 groups. In patients with AIA, as opposed to healthy subjects, aspirin challenge invariably precipitated a clinical reaction, accompanied in most patients by a further rise in plasma levels of PGD(2) metabolite and tryptase.
CONCLUSIONS: In stable AIA, though not in ATA, there is a steady release of PGD(2) into the blood, accompanied by the release of tryptase. Aspirin enhances this reaction in most patients. Release of bronchoconstrictive PGD(2) might contribute to the severe clinical course of AIA.

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Year:  2003        PMID: 12704352     DOI: 10.1067/mai.2003.1387

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  44 in total

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Review 2.  Update on Aspirin-Exacerbated Respiratory Disease.

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3.  Group 2 innate lymphoid cells are recruited to the nasal mucosa in patients with aspirin-exacerbated respiratory disease.

Authors:  Jacqueline J Eastman; Kellen J Cavagnero; Adam S Deconde; Alex S Kim; Maya R Karta; David H Broide; Bruce L Zuraw; Andrew A White; Sandra C Christiansen; Taylor A Doherty
Journal:  J Allergy Clin Immunol       Date:  2017-03-06       Impact factor: 10.793

4.  Comment on: "Targeting the PGD2/CRTH2/DP1 Signaling Pathway in Asthma and Allergic Disease: Current Status and Future Perspectives".

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5.  Eosinophils as a novel cell source of prostaglandin D2: autocrine role in allergic inflammation.

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6.  Thymic stromal lymphopoietin controls prostaglandin D2 generation in patients with aspirin-exacerbated respiratory disease.

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Review 7.  Aspirin-induced asthma: clinical aspects, pathogenesis and management.

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Journal:  Drugs       Date:  2004       Impact factor: 9.546

8.  Plasma 9alpha,11beta-PGF2, a PGD2 metabolite, as a sensitive marker of mast cell activation by allergen in bronchial asthma.

Authors:  G Bochenek; E Nizankowska; A Gielicz; M Swierczyńska; A Szczeklik
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Review 9.  The roles of the prostaglandin D(2) receptors DP(1) and CRTH2 in promoting allergic responses.

Authors:  R Pettipher
Journal:  Br J Pharmacol       Date:  2007-10-29       Impact factor: 8.739

Review 10.  Aspirin sensitivity and desensitization for asthma and sinusitis.

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Journal:  Curr Allergy Asthma Rep       Date:  2009-03       Impact factor: 4.806

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