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Artur Zembowicz, MD, PhD; Lucyna Mastalerz, MD; Malgorzata Setkowicz, MD; Waldemar Radziszewski, MD, PhD; Andrzej Szczeklik, MD

Arch Dermatol. 2003;139:1577-1582.

Background  Nonsteroidal anti-inflammatory drugs (NSAIDs) exacerbate various forms of urticaria by a nonallergic mechanism involving inhibition of cyclooxygenases.

Objectives  To assess safety of cyclooxygenase inhibitors in patients with chronic idiopathic urticaria (CIU) and NSAID sensitivity and to evaluate a role of cysteinyl leukotriene metabolism and mast cell activation in sensitivity to NSAIDs in CIU.

Design  Aspirin challenge test followed by randomized, prospective, double-blind, placebo-controlled crossover trial with cyclooxygenase 2 inhibitors.

Setting  Tertiary referral center of a university hospital.

Patients  Thirty-six patients with CIU.

Interventions  Aspirin challenge test (up to 500 mg); randomized trial with rofecoxib (up to 37.5 mg) and celecoxib (up to 300 mg) in aspirin-sensitive patients. After completion of the trial, 7 patients received naproxen sodium (500 mg) as a positive control.

Main Outcome Measures  Standardized skin examination, skin biopsy with mast cell count, urinary levels of leukotriene E₄ (LTE₄), and serum levels of mast cell tryptase.

Results  Aspirin induced skin eruption in 18 patients. Rofecoxib or celecoxib did not elicit skin eruption in any of the aspirin-sensitive patients. Patients with CIU had higher urinary excretion of LTE₄ than healthy control subjects. Basal urinary levels of LTE₄ and serum mast cell tryptase were increased in aspirin-sensitive compared with aspirin-tolerant patients. Severity and duration of aspirin-induced urticaria showed a positive correlation with urinary LTE₄ excretion. Naproxen precipitated urticaria in 5 of 7 aspirin-sensitive patients and caused further increase in urinary LTE₄.

Conclusions  Cyclooxygenase 2 inhibitors do not induce urticaria in patients with CIU sensitive to NSAIDs. Sensitivity to NSAIDs in CIU is associated with overproduction of cysteinyl leukotrienes and mast cell activation and most likely depends on inhibition of cyclooxygenase 1.

From the Department of Pathology, Harvard Medical School and Massachusetts General Hospital, Boston (Dr Zembowicz); Department of Medicine, Jagellonian University School of Medicine, Krakow, Poland (Drs Mastalerz, Setkowicz, and Szczeklik); and Merck Sharp and Dohme Idea Inc, Warszawa, Poland (Dr Radziszewski). Dr Radziszewski is an employee of Merck Sharp and Dohme Idea Inc.

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