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.

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.