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Prostaglandin E2 systemic production in asthma patients with and without aspirin hypersensitivity.
  1. Lucyna Mastalerz (lmastalerz{at}wp.pl)
  1. Jagiellonian University, Department of Medicine, Poland
    1. Marek Sanak (nfsanak{at}cyf-kr.edu.pl)
    1. Jagiellonian University, Department of Medicine, Poland
      1. Agnieszka Gawlewicz-Mroczka (aggaw{at}o2.pl)
      1. Jagiellonian University, Department of Medicine, Poland
        1. Adam Cmiel (mmszczek{at}cyf-kr.edu.pl)
        1. University of Science and Technology, Department of Applied Mathematics, Poland
          1. Anna Gielicz (mmszczek{at}cyf-kr.edu.pl)
          1. Jagiellonian University, Department of Medicine, Poland
            1. Andrew Szczeklik (mmszczek{at}cyf-kr.edu.pl)
            1. Jagiellonian University, Department of Medicine, Poland

              Abstract

              Rationale: Special regulatory role of prostaglandin E2 has been postulated in aspirin-induced asthma. Objectives: To investigate the effects of aspirin on systemic production of prostaglandin E2 and cysteinyl leukotrienes in patients with asthma.

              Methods: We determined urinary concentrations of: 1) two main prostaglandin E2 metabolites, i.e.:13,14-dihydro-15keto-PGE2 using commercial enzyme immunoassay and 9,15-dioxo-11α-hydroxy-2,3,4,5-tetranor-prostane-1,20-dioic acid using gas chromatography/mass spectrometry and 2) leukotriene E4 using immunoassay. Determinations were performed at baseline and following oral aspirin and celecoxib challenges, in two well-defined asthma phenotypes: aspirin-sensitive and aspirin-tolerant patients.

              Measurements and Main Results: Aspirin precipitated bronchial reactions in all aspirin-sensitive, but in none of the aspirin-tolerant patients. Celecoxib 400 mg was well tolerated by all patients except for one with aspirin-induced asthma. At baseline mean prostaglandin E2 metabolites values did not differ between the groups. Following different aspirin provocation doses, the two main prostaglandin E2 metabolites were decreased in the aspirin-tolerant group, but their mean level remained unchanged in the aspirin-sensitive group. The dose of aspirin had no effect on the magnitude of the response on the prostaglandin E2 metabolites and its duration. In both groups urinary prostaglandin E2 metabolites decreased following celecoxib challenge. No correlation was found between prostaglandin E2 metabolites and leukotriene E4.

              Conclusions: Aspirin-precipitated asthmatic attacks are not associated with changes in the systemic prostaglandin E2 production. In contrast, prostaglandin E2 systemic production becomes depressed by aspirin in non-sensitive patients. This different response might indicate COX-1 dependent prostaglandin E2 control of inflammatory cells in AIA. Thus, PGE2 is released during the clinical reactions to aspirin through an alternate COX-2 pathway. Clinical implications of this finding are in line with current observations of good tolerance of the selective COX-2 inhibitors in sensitive patients.

              • Aspirin-induced asthma
              • aspirin-tolerant asthma
              • cyclooxygenase
              • eicosanoids
              • lipoxygenase

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