Objective: We aimed to investigate systemic production of prostaglandin E2 in chronic idiopathic urticaria patients, stratified by positive or negative clinical reaction during oral aspirin challenge.

Materials and Methods: Urinary concentrations of semi-stable prostaglandin E2 metabolite, 13,14- dihydro-15-keto-PGE2, were measured using commercial enzyme immunoassay at baseline and following aspirin challenge.

Results: Aspirin precipitated skin reactions in 14 (63.6%) out of 22 patients with chronic idiopathic urticaria. At baseline, mean urinary prostaglandin E2 metabolite values did not differ between patients who reacted to the drug and those who tolerated it. Following aspirin administration, urinary prostaglandin E2 metabolite excretion significantly decreased in all patients. No correlation was found between urinary prostaglandin E2 metabolite excretion and dose of aspirin precipitating hypersensitivity symptoms.

Conclusion: Administration of aspirin decreases systemic production of prostaglandin E2 in chronic idiopathic urticaria patients. This effect is independent of the outcome of aspirin challenge and does not discriminate between patients who develop hypersensitivity symptoms and those who tolerate aspirin well.